Biochemical And Biophysical Research Communications[JOURNAL]
Sun
200 papers
BP-1-102 inhibits multiple pathways of NFATc1 activation to alleviate osteoporosis and downregulate osteoclast differentiation in ovariectomized mice.
Yang J, Chen L, Gan G … +5 more , Qi J, Zhang L, Han S, Kong J, Wang N
Biochem Biophys Res Commun · 2026 May · PMID 42308767 · Publisher ↗
Signal transducer and activator of transcription 3 (STAT3) activates nuclear factor of activated T cells 1 (NFATc1), a key regulator of osteoclastogenesis. This study investigated the STAT3 inhibitor BP-1-102 in receptor...
Signal transducer and activator of transcription 3 (STAT3) activates nuclear factor of activated T cells 1 (NFATc1), a key regulator of osteoclastogenesis. This study investigated the STAT3 inhibitor BP-1-102 in receptor activator of nuclear factor kappa-B ligand (RANKL)-induced osteoclast differentiation from bone marrow macrophages (BMMs). BP-1-102 (2.5/5 μM) suppressed osteoclast formation and specific gene expression without cytotoxicity, while inhibiting STAT3 phosphorylation and NFATc1. Gene ontology analysis revealed enrichment in osteoclast differentiation and mitogen-activated protein kinase (MAPK) pathways. BP-1-102 downregulated the c-Fos/NFATc1 axis by suppressing MAPK and NF-κB signaling. In ovariectomized mice, BP-1-102 attenuated bone loss, reduced osteoclast numbers (≥3 nuclei), and inhibited STAT3/p38 phosphorylation. In summary, BP-1-102 rescues bone loss by targeting p-STAT3/MAPK/NF-κB signaling, demonstrating therapeutic potential for osteoporosis.
HSP90 is involved in curcumin-mediated inhibition of tau aggregation.
Kam MK, Kim JW, Choi JY … +2 more , Koh YH, Jo C
Biochem Biophys Res Commun · 2026 Jun · PMID 42308766 · Publisher ↗
Tau aggregation in neurons is a pathological hallmark of Alzheimer's disease (AD). The development of therapeutic drugs that inhibit tau aggregation in tauopathies, including AD, remains challenging. Herein, we developed...
Tau aggregation in neurons is a pathological hallmark of Alzheimer's disease (AD). The development of therapeutic drugs that inhibit tau aggregation in tauopathies, including AD, remains challenging. Herein, we developed a tau self-interaction reporter system using split Nanoluciferase (Tau-NLuc) in which luciferase activity is restored by the self-assembly of split Nanoluciferases following self-interaction between tau proteins. Curcumin (CCM), a phenolic organic compound, significantly reduced luciferase activity in the Tau-NLuc system, including mutant tau forms such as S396/404E and P301L, which are known aggregation-prone tau forms, suggesting that CCM may act as a potential inhibitor of tau aggregation. CCM did not alter the protein levels of phosphorylated tau as well as total tau, indicating that the reduction in luciferase activity by CCM did not originate from tau degradation, but rather from tau aggregation inhibition. Of note, CCM significantly increased heat shock protein (HSP) 90 dimer. The reduced luciferase activity in the Tau-NLuc system by CCM was recovered by knockdown of the HSP90 gene using a siRNA specific for HSP90 or treatment of an inhibitor of HSP90 NCT-58, supporting the involvement of HSP90. Intriguingly, hexahydrocurcumin (HHC), a derivative of CCM, did not reduce luciferase activity, nor did it induce the formation of the HSP90 dimer, suggesting that HSP90 dimer formation may contribute to the CCM-mediated inhibition of tau aggregation. Taken together, the results demonstrate that CCM inhibits tau aggregation with the involvement of HSP90, providing novel insights into the development of therapeutic strategies for AD.
A TRIM28-MCM7 regulatory axis sustains DNA replication programs in glioblastoma.
Hu X, Yang L, Cui H
Biochem Biophys Res Commun · 2026 Jun · PMID 42308765 · Publisher ↗
Aberrant activation of DNA replication programs is essential for Glioblastoma cell proliferation, but the upstream mechanisms that maintain replication competence remain poorly defined. Here, we identify TRIM28 as a mult...
Aberrant activation of DNA replication programs is essential for Glioblastoma cell proliferation, but the upstream mechanisms that maintain replication competence remain poorly defined. Here, we identify TRIM28 as a multilayered regulator of DNA replication in Glioblastoma. TRIM28 was highly expressed in Glioblastoma tissues, increased with tumor grade, and predicted poor prognosis. The enrichment analysis linked TRIM28-high tumors to DNA replication-related pathways, and TRIM28 depletion impaired BrdU incorporation and CldU-labeled replication activity in Glioblastoma cells. Integrated analyses of Glioblastoma datasets identified MCM7, a core component of the MCM2-7 replicative helicase complex, as a TRIM28-associated replication factor. MCM7 was upregulated in Glioblastoma, positively correlated with TRIM28, and associated with unfavorable clinical outcome. Mechanistically, TRIM28 occupied the MCM7 promoter and enhanced its transcriptional activity, as supported by public ChIP-seq data, promoter reporter assays, and ChIP-qPCR validation. In parallel, TRIM28 interacted with MCM7 and promoted its K63-dependent ubiquitination. These findings reveal a TRIM28-MCM7 axis that supports DNA replication-associated proliferation through transcriptional activation and K63-dependent post-translational regulation.
Thapsigargin-induced autophagic flux impairment and inflammation are potentiated by CLN3 deficiency and alleviated by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) in human ARPE-19 cells.
Torsti T, Hytti M, Toppila M … +2 more , Forsberg MM, Kauppinen A
Biochem Biophys Res Commun · 2026 Jun · PMID 42308764 · Publisher ↗
Juvenile neuronal lipofuscinosis (JNCL) is a rare disease caused by mutations in the CLN3 gene. It leads to early vision loss mediated by retinal degeneration. Impaired autophagosomal-lysosomal degradation is a major hal...
Juvenile neuronal lipofuscinosis (JNCL) is a rare disease caused by mutations in the CLN3 gene. It leads to early vision loss mediated by retinal degeneration. Impaired autophagosomal-lysosomal degradation is a major hallmark of JNCL pathology, and neuroinflammation has also been postulated to play a role in its pathogenesis. Thapsigargin, a selective inhibitor of sarco/endoplasmic reticulum Ca-ATPase, inhibits autophagy, leading to an accumulation of autophagosomes/autophagophores in cells. Cells with defective CLN3 protein function have been found to be particularly sensitive to the anti-autophagic effects of thapsigargin. Here, we characterized the effects of thapsigargin on inflammatory cytokines and autophagic markers in ARPE-19 cells using ELISA and western blotting. We further examined these effects in cells deficient in CLN3 function by exposing the cells to CLN3 siRNA and testing whether the effects of thapsigargin could be modulated by the well-known autophagy activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR). Thapsigargin induced the accumulation of LC3 and p62/SQSTM1, consistent with impaired autophagic flux in ARPE-19 cells. Additionally, we observed that thapsigargin possessed pro-inflammatory potential, as it induced the release of IL-6 in ARPE-19 cells, no inflammasome activation was detected. Both effects were enhanced by CLN3 siRNA and alleviated by AICAR. In conclusion, thapsigargin-induced impaired autophagic flux and the accompanying inflammatory response are more pronounced in CLN3-deficient ARPE-19 cells, indicating that loss of CLN3 function affects both autophagy and inflammatory signaling.
Spectral characteristics and fluorescence of lycopene from a purple-colored Microbacterium albipurpureum ET2.
Klementiev KE, Volynchikova EA, Fangfang W … +2 more , Pirutin SK, Tsavkelova EA
Biochem Biophys Res Commun · 2026 Jun · PMID 42308763 · Publisher ↗
A recently described novel species of Microbacterium albipurpureum ET2, isolated from the aerial roots of a leafless orchid, revealed strong plant growth-promoting activities. It also showed unique pigmentation, changing...
A recently described novel species of Microbacterium albipurpureum ET2, isolated from the aerial roots of a leafless orchid, revealed strong plant growth-promoting activities. It also showed unique pigmentation, changing from white-yellowish to bright purple. In this study, using genome mining, the strain was found to possess a non-mevalonate biosynthetic pathway and the genes responsible for С40 carotenoid production. Several biosynthetic gene clusters (BGC) were predicted by antiSMASH, including a terpene synthesis-encoding one, consisting of seven genes with structural and sequence similarity to known BGCs. The core crtEBI genes for lycopene biosynthesis are clustered together in the genome. Biosynthesis of lycopene was confirmed by mass-spectrometry in both purple and yellowish cultures. Complementary spectroscopic techniques, such as Raman, UV-Vis, and fluorescence spectroscopy, also revealed the presence of lycopene and its precursor, phytoene. Fluorescence from S2 sub-energy levels, with lifetimes of 0.8 ns, 3.2 ns, and 9.0 ns, determined by time-correlated single photon counting, was detected. Narrowing Raman peak shifts by FWHM reach 15-22% for the purple-colored culture compared to yellowish one, suggesting aggregation of lycopene molecules.
MicroRNA-300-3p promotes cardiac hypertrophy by modulating the ACOX-1/GPX4 pathway.
Li X, Wang Y, Yang Z … +7 more , Li X, Li X, Li Z, Xu X, Xu J, Gu J, Yang X
Biochem Biophys Res Commun · 2026 Jun · PMID 42302381 · Publisher ↗
Cardiac hypertrophy (CH) represents a key pathological process in cardiac remodeling and progression toward heart failure. Understanding its underlying molecular mechanisms is essential for developing novel therapeutic s...
Cardiac hypertrophy (CH) represents a key pathological process in cardiac remodeling and progression toward heart failure. Understanding its underlying molecular mechanisms is essential for developing novel therapeutic strategies. MicroRNAs (miRNAs) play crucial regulatory roles in cardiovascular diseases, however, their specific involvement in CH remains incompletely understood. Here, we demonstrate that miR-300-3p modulates angiotensin II (Ang II)-induced CH through the ACOX1/GPX4 pathway. Functionally, miR-300-3p directly targets ACOX1, leading to its downregulation and subsequent enhancement of ferroptosis. Overexpression of ACOX1 reversed these effects. Mechanistically, hypomethylation of the miR-300-3p promoter region, mediated by DNMT1, elevated miR-300-3p expression and contributed to Ang II-induced hypertrophic responses. Furthermore, ACOX1 exerted anti-hypertrophic effects via activation of the GPX4 signaling pathway. In conclusion, DNMT1-regulated promoter hypomethylation enhances miR-300-3p expression, suppresses ACOX1, and promotes ferroptosis in Ang II-induced CH. The miR-300-3p/ACOX1/GPX4 axis uncovers novel molecular pathways in CH and identifies potential therapeutic regulators.
SlMYBR5 shows preliminary evidence as a negative regulator of tomato fruit ripening by modulating metabolic pathways.
Li C, Fan Y, Guo C
Biochem Biophys Res Commun · 2026 Jun · PMID 42302380 · Publisher ↗
Fruit ripening in tomato (Solanum lycopersicum L.) is a complex, genetically regulated process that determines final fruit quality. Through transcriptomic profiling of three ripening stages-green-ripening (GR), breaker (...
Fruit ripening in tomato (Solanum lycopersicum L.) is a complex, genetically regulated process that determines final fruit quality. Through transcriptomic profiling of three ripening stages-green-ripening (GR), breaker (BR), and red-ripening (RR)-we identified an RR-upregulated MYB transcription factor, SlMYBR5. Functional studies demonstrated that SlMYBR5 knockout accelerates ripening, while its overexpression delays it. RNA-seq analysis revealed that differentially expressed genes (DEGs) in the slmybr5 mutant were primarily associated with enzyme activity, secondary metabolism, and carbohydrate metabolism. In contrast, DEGs in the SlMYBR5-OE line were enriched in amino acid metabolism and photosynthesis. Further phenotypic analysis showed that slmybr5 mutants exhibited higher chlorophyll content at the GR stage and accumulated the highest carotenoid levels at the RR stage, whereas SlMYBR5-OE lines displayed reduced pigmentation. Moreover, overexpression of SlMYBR5 led to significant reductions in fruit length and width, although fruit weight was not significantly affected. Collectively, our findings preliminarily establish SlMYBR5 as a key regulator of tomato fruit ripening, acting through the modulation of metabolic pathways, pigmentation, and fruit morphology, thereby revealing a novel layer of metabolic control in the ripening regulatory network.
Elucidation of the molecular binding mechanism of an anticancer thiolato-bridged manganese(I) carbonyl complex with apotransferrin: Thermodynamic and structural insights.
Anil A, Tripathi D, Nayak SS … +4 more , Krishna R, Kumar U, Manimaran B, Sakthivel N
Biochem Biophys Res Commun · 2026 Jun · PMID 42296687 · Publisher ↗
We investigated the molecular binding of an anticancer thiolato-bridged manganese(I) carbonyl metallacycle (S-MnC) to apotransferrin (ApoTf) through biophysical and computational approaches. UV-Vis spectroscopy results r...
We investigated the molecular binding of an anticancer thiolato-bridged manganese(I) carbonyl metallacycle (S-MnC) to apotransferrin (ApoTf) through biophysical and computational approaches. UV-Vis spectroscopy results revealed hyperchromism, indicative of the interaction between ApoTf and S-MnC. Fluorescence quenching demonstrated increasing Stern-Volmer constants and quenching rate constants with temperature (300 - 312 K), confirming dynamic quenching. Time resolved fluorescence showed average lifetime reduction from 2.67 to 2.05 ns. The distance between the ApoTf (donor) and S-MnC (acceptor) obtained based on fӧrster resonance energy transfer (FRET) suggests a high efficiency of energy transfer corresponding to an effective average encounter distance (r) of 3.21 nm, consistent with transient collisional interactions characteristic of dynamic quenching. Thermodynamic analysis revealed positive ΔH° and ΔS° with negative ΔG° values, indicating entropy driven, spontaneous binding via hydrophobic interactions. CD spectroscopy showed modest secondary structural alterations. Molecular docking localized S-MnC in the N-lobe iron binding pocket with hydrogen bonding to Y95 (a Fe coordinating residue), along with several hydrophobic interactions and a predicted binding energy of -10.2 kcal mol. S-MnC forms a stable, thermodynamically favourable complex with ApoTf near iron coordination cleft, suggesting exploitation of transferrin mediated endocytosis as a mechanism for cellular delivery.
Lack of Chloride Intracellular Channels (CLICs) confers resistance to hypoxia in Drosophila melanogaster via differential regulation of ERK and AKT pathways.
Spitnale S, Seeley S, Oyetunji I … +6 more , Lam A, Sutherland M, Tanda S, Berryman M, Singh H, Gururaja Rao S
Biochem Biophys Res Commun · 2026 Jun · PMID 42296686 · Publisher ↗
Ion channels are critical regulators of cellular excitability, ionic homeostasis, and signal transduction, playing essential roles in cellular adaptation to hypoxic stress. Among these, intracellular chloride channels (C...
Ion channels are critical regulators of cellular excitability, ionic homeostasis, and signal transduction, playing essential roles in cellular adaptation to hypoxic stress. Among these, intracellular chloride channels (CLICs) represent a unique subclass of chloride channels predominantly localized to intracellular organelles. Given their established roles in redox-regulation and transcriptional responsiveness to hypoxia, we investigated the hypoxic responses in Drosophila melanogaster, which possesses a single CLIC homolog. We subjected CLIC-null mutant flies to hypoxic stress and observed significantly enhanced resistance to hypoxia-induced damage compared to wild-type controls. Remarkably, acute hypoxic exposure followed by reoxygenation did not impair cardiac function in CLIC mutant flies, whereas wild-type flies exhibited notable cardiac dysfunction. Mutant flies also demonstrated improved overall survival under hypoxic conditions. To elucidate the underlying mechanisms of this protective phenotype, we assessed molecular markers and found consistent downregulation of ERK expression at the transcript, total protein, and phosphorylated levels in CLIC-mutant flies. Histological analysis revealed preserved myocardial fiber architecture in mutants, in contrast to the structural disarray observed in wild-type hearts. Furthermore, we detected upregulation of pro-survival signaling, particularly the AKT pathway, evidenced by increased AKT phosphorylation. This effect was abolished upon pharmacological inhibition with rapamycin. Collectively, our findings suggest that Drosophila CLIC proteins contribute to maladaptive cardiac remodeling and suppression of cytoprotective signaling under hypoxic stress. Inhibition of CLIC function appears to confer cardioprotection and enhance organismal survival in hypoxic environments, highlighting a potential therapeutic target for ischemic heart disease.
Renal tubular epithelial-derived Angptl4 promotes renal fibrosis by inducing tubular cell senescence.
Li H, Zhu Z, Li P … +6 more , Shen Q, Wu Y, Yang M, Ma X, Lu D, Gong W
Biochem Biophys Res Commun · 2026 Aug · PMID 42289177 · Publisher ↗
Chronic kidney disease (CKD) is a global public health issue affecting over 10% of the adult population. Irrespective of disease aetiology, kidney fibrosis is a common pathological progression of CKD, characterized by ex...
Chronic kidney disease (CKD) is a global public health issue affecting over 10% of the adult population. Irrespective of disease aetiology, kidney fibrosis is a common pathological progression of CKD, characterized by excessive extracellular matrix deposition within the kidney parenchyma. However, the pathogenesis of renal fibrosis remains poorly understood, and treatment options are limited. Here, we identify upregulated expression of Angptl4 in renal tubular epithelial cells (RTECs) of CKD patients, as well as in mice with renal fibrosis and aging mice. Genetic knockout of Angptl4 attenuates renal fibrosis and RTEC senescence, whereas overexpression of Angptl4 in RTECs exacerbates both renal fibrosis and RTEC senescence. Mechanistically, Angptl4 derived from RTECs binds to integrin β1 (Itgb1), thereby activating focal adhesion kinase (Ptk2/FAK) and promoting RTEC senescence. Additionally, fibroblasts are activated by the senescence-associated secretory phenotype from Angptl4 overexpressed RTECs to secrete extracellular matrix protein, causing renal fibrosis. Together, our study delineates the roles of RTEC-derived Angptl4 in renal fibrosis, proposing a novel therapeutic strategy for intervening in CKD and renal fibrosis.
Mechanism of berberine in the treatment of polycystic ovary syndrome revealed by network pharmacology analysis: Focusing on ferroptosis, ROS, immunity and inflammation.
Ye K, Liu L, Fang J … +6 more , Tian M, Han X, Chen X, Wang D, Liu Y, Xia Q
Biochem Biophys Res Commun · 2026 Aug · PMID 42289176 · Publisher ↗
Berberine, a bioactive component isolated from traditional Chinese medicine, functions as a multitarget regulator and has been proven to ameliorate reproductive endocrine disorders and metabolic abnormalities in patients...
Berberine, a bioactive component isolated from traditional Chinese medicine, functions as a multitarget regulator and has been proven to ameliorate reproductive endocrine disorders and metabolic abnormalities in patients with polycystic ovary syndrome (PCOS). Nevertheless, the exact molecular mechanisms underlying its therapeutic effects remain to be fully elucidated. In this study, we integrated multi-omics data analysis with in vitro experimental validation. Differentially expressed genes associated with PCOS were screened from the Gene Expression Omnibus (GEO) database, and berberine-targeted genes were retrieved from public databases to construct a protein-protein interaction (PPI) network. KGN and Ishikawa cell models were employed to verify the regulatory effects of berberine on cell proliferation, oxidative stress and nuclear receptor signaling. Finally, molecular docking and molecular dynamics simulations were performed to analyze the binding patterns, so as to comprehensively decipher the molecular mechanism of berberine against PCOS. A total of 32 common targets were identified via network pharmacology analysis, which were mainly enriched in metabolism-, reproduction- and inflammation-related signaling pathways. Further screening identified 8 hub genes that constituted a nuclear receptor-kinase interaction module. Enrichment analysis indicated that these hub genes were cell-specifically correlated with N6-methyladenosine (mA) modification, ferroptosis and immune inflammation. In vitro cellular assays demonstrated that berberine suppressed cell proliferation, elevated reactive oxygen species (ROS) levels and reduced intracellular iron concentrations. Molecular simulation results revealed the favorable binding energy of berberine to target receptors and stable RMSD values of the ligand-receptor complexes, uncovering a multi-axis network regulatory mechanism of berberine. Collectively, this study adopts an integrated multi-method strategy and confirms that berberine targets the nuclear receptor-kinase interaction module. It exerts multi-axis regulatory effects on PCOS by modulating mA modification, ferroptosis, ROS accumulation and immune inflammatory responses.
Comparative assessment of behavioral and systemic effects of small (10 nm) and large (100 nm) tellurium nanoparticles in a chronic mouse model.
Rogachev VV, Goltyaev MV, Varlamova EG … +3 more , Baimler IV, Gudkov SV, Turovsky EA
Biochem Biophys Res Commun · 2026 Aug · PMID 42288038 · Publisher ↗
This study presents a comparative evaluation of the behavioral and systemic effects of small (10 nm) and large (100 nm) tellurium nanoparticles (TeNPs) obtained by laser ablation in a chronic in vivo experiment on male B...
This study presents a comparative evaluation of the behavioral and systemic effects of small (10 nm) and large (100 nm) tellurium nanoparticles (TeNPs) obtained by laser ablation in a chronic in vivo experiment on male BALB/c mice. TeNPs were administered intraperitoneally at doses of 2.5 and 5 μg/g either acutely (single injection) or chronically (four injections weekly for 5 weeks, totaling 20 injections). Spontaneous locomotor activity was recorded continuously for 72 h using a piezoelectric actometry, while body weight dynamics, organ coefficients, histopathology (heart, kidney, liver), and gene expression profiles (redox status, inflammation, apoptosis) were assessed. The 100 nm TeNPs induced persistent hyperlocomotion (activity up to 15 h/day), disrupted circadian rhythms, and caused progressive body weight loss during chronic administration. In contrast, 10 nm TeNPs produced only transient behavioral changes at 2.5 μg/g and no significant alterations at 5 μg/g in the chronic setting. Histological analysis revealed no overt morphological damage in the heart, kidneys, or liver, except for occasional hyaline casts in renal tubules and mild sinusoidal congestion in the liver after high-dose 100 nm TeNPs. Molecular profiling showed tissue-specific changes: in the heart, 10 nm TeNPs upregulated catalase, IL-1β, and IL-6 while downregulating Nox1; in the kidneys and liver, 100 nm TeNPs activated pro-inflammatory and pro-oxidant genes (Nox1, Nox2, IL-6, Tnfα, ATF-6) and reduced IL-10 and Bcl-xL. However, these molecular shifts did not translate into histologically detectable organ toxicity. Thus, particle size critically determines the biological response: 100 nm TeNPs exert pronounced behavioral and systemic effects, whereas 10 nm TeNPs demonstrate a more favorable safety profile although the mechanisms (direct CNS versus peripheral) remain to be investigated. The absence of significant morphological lesions under the tested regimens suggests that histologically detectable organ damage is unlikely. The absence of significant morphological lesions under the tested regimens indicates a low toxic potential of these TeNPs.
Ameliorating effects of Coenzyme Q10 and its nanosuspension against cyclophosphamide-induced hepatoxicity in rats.
Saeed HY, Orabi SH, Mansour DA … +3 more , Korany RMS, Alsofany JM, Mousa AA
Biochem Biophys Res Commun · 2026 Aug · PMID 42288037 · Publisher ↗
BACKGROUND: Coenzyme Q10 (CoQ10) is a natural antioxidant. In present study aims to evaluate the possible hepatoprotective effects against experimentally induced cyclophosphamide (CP) hepatotoxicity in rats. METHODS: In...
BACKGROUND: Coenzyme Q10 (CoQ10) is a natural antioxidant. In present study aims to evaluate the possible hepatoprotective effects against experimentally induced cyclophosphamide (CP) hepatotoxicity in rats. METHODS: In total, 56 male albino rats were randomly distributed into 7 groups (n = 8). G1 (control saline); G2: (control corn oil group); G3: received CoQ10 (15 mg/kg orally) (100% purity) every 48 h for 4 weeks; G 4: administrated CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks; G5: received single injection of CP (150 mg/kg i.p) (1 g vial); G6: was treated with CoQ10 (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p); G7: was treated with CoQ10-NS (15 mg/kg orally) every 48 h for 4 weeks after CP (150 mg/kg i.p). Serum and hepatic tissue samples were obtained for biochemical analysis as well as histopathological evaluation. RESULTS: The optimized formulation of CoQ10-NS (1.2% Poloxamer 407) showed particle size, polydispersity index, and zeta potential of 217.033 ± 2.650 nm, 0.274 ± 0.024, and -24.233 ± 0.777 mV, respectively, and excellent physical and chemical stability. Experimentally induced liver damage in the CP-injected rat group was evidenced by the increase of serum ALT and AST activities, elevated hepatic concentrations of malondialdehyde (MDA), decreased activity of hepatic glutathione peroxidase (GPx), and increased hepatic IL-6 and TNF-alpha levels. Alongside, CP induced histopathological changes with increased immune expression of Bax and caspase 3, and decreased Bcl-2 compared to the control groups. Meanwhile, CoQ10 and CoQ10-NS reversed all pathophysiological alterations induced by CP. CONCLUSION: CoQ10 and CoQ10-NS showed ameliorative effects against the hepatic cytotoxicity induced by CP in rats, elucidating anti-inflammatory and anti-apoptotic properties with a marked superiority of CoQ10-NS to crude CoQ10 as a result of nanosizing and enhanced bioavailability.
B cells promote the growth and stem-like qualities of breast cancer cells in the bone marrow.
Sasaki SI, Fitria Wahyuniputri R, Tanabe Y … +4 more , Zhou Y, Terashima Y, Sakurai H, Hayakawa Y
Biochem Biophys Res Commun · 2026 Aug · PMID 42288036 · Publisher ↗
Bone metastasis is a critical factor in the morbidity and mortality of breast cancer patients, yet the specific contributions of the bone marrow microenvironment to this process remain incompletely understood. We investi...
Bone metastasis is a critical factor in the morbidity and mortality of breast cancer patients, yet the specific contributions of the bone marrow microenvironment to this process remain incompletely understood. We investigated the influence of bone marrow cell populations on intraosseous tumor growth following the injection of E0771 breast cancer cells into the bone. Kinetic analysis revealed a progressive reduction in CD19CD20B220 immature B cells as the tumor burden increased. Depletion of CD20 immature B cells, but not CD19CD20B220 pro/pre-B cells, significantly increased the intraosseous tumor burden along with upregulation of the proliferation marker Ki-67. To simulate the bone cavity environment, we employed anchorage-independent in vitro co-cultures of tumor cells with B-cell populations. Using this co-culture system, pro/pre-B cells, but not immature B cells, enhanced tumor cell proliferation with upregulation of Ki-67. Mechanistically, pro/pre-B cells enhanced tumor cell proliferation through the production of soluble factors and promoted stem cell-like properties, as indicated by increased expression of the stem cell marker CD44. By analyzing clinical datasets from breast cancer patients, we found that high CD20 expression correlated with longer overall survival, thereby supporting a positive correlation between increased immature B cells and better control of disease progression. Collectively, these results indicate contradictory roles for CD20 pro/pre-B cells and CD20 immature B cells in controlling the tumor microenvironment in bone.
Dynamic switching of macrophage phagocytic polarity between opposing targets.
Noumi K, Kato S, Yasuda K
Biochem Biophys Res Commun · 2026 Aug · PMID 42288035 · Publisher ↗
How macrophages reprioritize competing phagocytic targets under persistent spatial competition remains unclear. Here, using a dual-microneedle assay in which opposite sides of a single macrophage were sequentially stimul...
How macrophages reprioritize competing phagocytic targets under persistent spatial competition remains unclear. Here, using a dual-microneedle assay in which opposite sides of a single macrophage were sequentially stimulated, we examined how phagocytic polarity established toward one target is redistributed when an opposing target continues to compete. Membrane extension did not converge on stable dual extension after contact with the second opsonized microneedle. Instead, dominance switched reciprocally between the two phagocytic fronts, and the same pattern was reproducibly observed in five additional cells. Local cross-correlation analysis showed that anti-phase coupling between the two fronts was enriched within switching windows, whereas non-switching intervals showed weaker or qualitatively different coupling. These switching windows were also associated with opposite directional biases in cell velocity, consistent with coupling between local front switching and whole-cell movement polarity. These findings support a multiphase switching process in which macrophage phagocytic polarity remains dynamically reconfigurable under persistent competition between opposing targets.
Non-canonical Platelet activation by oral squamous cell carcinoma extracellular vesicles through cooperative thrombin formation.
Chen R, Jin G, McIntyre TM
Biochem Biophys Res Commun · 2026 Aug · PMID 42284996 · Publisher ↗
Coagulation contributes to cancer mortality, and tumor cells activate platelets to release growth factors. However, this activation is non-canonical, employs unknown agonists and, uniquely, is not immediate. Platelets ar...
Coagulation contributes to cancer mortality, and tumor cells activate platelets to release growth factors. However, this activation is non-canonical, employs unknown agonists and, uniquely, is not immediate. Platelets are activated by human cell lines derived from Oral Squamous Cell Carcinomas (OSCC) with this atypical delay. The stimulatory activity was not a soluble factor, but rather was completely recovered in spontaneously shed extracellular vesicles (EV). EV did not contain established platelet agonists. Instead, chemical and pharmacologic inhibitors show OSCC EV interacted with quiescent platelets to assemble extrinsic and common coagulation complexes that generated thrombin after a significant delay. Newly generated thrombin then stimulated platelets through their PAR1 thrombin receptor. Translocation of intracellular phosphatidylserine to the platelet surface, enabled by its enzymatic oxidation, is essential for de novo formation of coagulation complexes. The delay in OSCC EV-induced platelet aggregation correlated to the delay in phosphatidylserine surface expression. Platelets express the oxidant-generating prorenin receptor (p)RR, while OSCC-EV contained its prorenin ligand. (p)RR non-proteolytically activates the prorenin zymogen and blockade of either this interaction by the decoy PRO20 peptide or inhibition of renin activity suppressed phosphatidylserine translocation and platelet activation. OSCC EV induced delayed peroxidation of platelet membrane lipids, while the intra-membranous radical trap Liproxstatin-1 suppressed phospholipid oxidation, phosphatidylserine display, and platelet activation. We conclude hysteresis characteristic of non-canonical, tumor cell-induced platelet activation reflects a novel time-dependent process of pro-thrombin activation. The rate-limiting step is membrane oxidation that enables phosphatidylserine translocation to the platelet surface and subsequent formation of the premier platelet agonist, thrombin.
Understanding antimicrobial resistance phenotype in Indian clinical isolates through genomic lens.
Aggarwal R, Das A, Kaur J … +1 more , Bhardwaj A
Biochem Biophys Res Commun · 2026 Aug · PMID 42284995 · Publisher ↗
Antimicrobial Resistance (AMR) poses a global health crisis, with a disproportionately higher burden in developing countries. Yet, the genome-wide exploration of bacterial resistance in high-burden countries like India r...
Antimicrobial Resistance (AMR) poses a global health crisis, with a disproportionately higher burden in developing countries. Yet, the genome-wide exploration of bacterial resistance in high-burden countries like India remains limited due to underrepresentation of high-quality data in publicly available resources. Integrating whole-genome sequencing (WGS) data with standardised phenotypic data, enables characterization of local resistome patterns. In this study, a systematic workflow has been implemented to curate WGS and associated AST data from Indian isolates of critical WHO bacterial priority pathogens. Assembled genomes and curated data were evaluated as per global standards of EUCAST and CLSI. Genomic analyses were performed to identify insertion elements and antibiotic resistance genes (ARGs), correlate presence of ARGs with AST phenotype, and compare the resistomes with global genome datasets for the priority drug-bug combinations. A total of 871 non-redundant AST-linked isolates were curated including A. baumannii (n = 119), E. coli (n = 305) and K. pneumoniae (n = 447) from 75 literature studies, BV-BRC and AST browser. The curated Indian isolates were resistant to many 'Watch' category antibiotics indicating strong reliance on last-resort antibiotics. It was observed that Indian samples are enriched in a small set of resistance determinants like bla, blaand blaA. baumannii and bla, bla, bla in E. coli and K. pneumoniae, while the global dataset has a broader diversity of ARGs. It is also observed that isolates have more than one resistance mechanism, pointing to AMR being a complex phenotype. ARG co-occurrence networks provide a framework to analyze the complex molecular interactions leading to emergence of AMR. This study highlights the local AMR trends in Indian clinical isolates and provides recommendations for standardized data reporting that are also applicable globally.
β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.
Zhang L, Kong X, Hong G … +2 more , Zheng Y, Zang L
Biochem Biophys Res Commun · 2026 Aug · PMID 42284994 · Publisher ↗
OBJECTIVE: To investigate the effect of β-Sitosterol on interleukin (IL)-1β-induced chondrocyte injury and the related mechanism. METHODS: An osteoarthritis model was constructed by treating immortalized human cartilage...
OBJECTIVE: To investigate the effect of β-Sitosterol on interleukin (IL)-1β-induced chondrocyte injury and the related mechanism. METHODS: An osteoarthritis model was constructed by treating immortalized human cartilage cells with IL-1β. The identity and purity of β-Sitosterol were confirmed by FTIR, H NMR, C NMR, RP-HPLC-ELSD, and UPLC-MS before cell experiments. The optimal concentrations of IL-1β and β-Sitosterol for treating cells were determined by qPCR and CCK8 assay. The cells were divided into three groups: Control group, Model group, and Model+β-Sitosterol group. Cell viability was detected by CCK8 assay. The mRNA expression of IL-18, IL-1β and tumor necrosis factor-α (TNF-α) was detected by qPCR. Collagen type II alpha 1 chain (COL2A1) and matrix metalloproteinase 13 (MMP13) expression was detected by immunofluorescence. Reactive oxygen species (ROS) and mitochondrial membrane potential were detected by flow cytometry. Malondialdehyde (MDA), Glutathione (GSH) and Fe were detected by ELISA and biochemical test. Mitochondrial structure was observed by transmission electron microscopy, and the protein expression of ferroptosis related factors was detected by Western blot. RESULTS: After induction of chondrocytes with IL-1β, the cell viability was decreased, the gene expression of inflammatory cytokines was increased, the proportion of cells with reduced ROS content and mitochondrial membrane potential were increased, MDA and Fe content were increased, and GSH content was decreased. Mitochondrial structure showed ferroptosis-like changes. The expression of COL2A1, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), total nuclear factor erythroid 2-related factor 2 (NRF2), and nuclear NRF2 was decreased. MMP13, ANO6, and p-p38/p38 levels were increased. Treatment of chondrocytes with β-Sitosterol could reverse these changes induced by IL-1β. CONCLUSION: Spectrally confirmed, high-purity β-Sitosterol alleviated IL-1β-induced chondrocyte injury by suppressing inflammatory activation, extracellular matrix degradation, mitochondrial dysfunction, and ferroptosis-related oxidative damage, suggesting its potential as a candidate compound for osteoarthritis intervention.
Oxyresveratrol induces ER stress and growth inhibition associated with glutathione depletion in breast cancer cells.
Ohmine N, Ikematsu S, Yamamoto T
Biochem Biophys Res Commun · 2026 Aug · PMID 42284993 · Publisher ↗
Polyphenolic stilbene oxyresveratrol (OXYRES) is produced by various plant species. It exhibits a wide range of biological activities, including anti-inflammatory, anticancer, antibacterial, and anti-melanogenic activiti...
Polyphenolic stilbene oxyresveratrol (OXYRES) is produced by various plant species. It exhibits a wide range of biological activities, including anti-inflammatory, anticancer, antibacterial, and anti-melanogenic activities. However, the molecular mechanisms underlying these effects are not well understood. In this study, we demonstrate that OXYRES inhibits the proliferation of MCF-7 human breast cancer cells in a dose-dependent manner. Additionally, OXYRES induces apoptosis, autophagy, and cell cycle arrest in MCF-7 cells. Our data suggest that these processes involve the unfolded protein response (UPR) associated with endoplasmic reticulum (ER) stress. Importantly, we found that a decrease in intracellular glutathione (GSH) levels may mediate these effects independently of reactive oxygen species (ROS) production.
Synthesis and multipurpose efficacy of novel PrSmZnO nanoparticles: Antibacterial, cytotoxic and photocatalytic activities.
Jasmine A, Baskaran P, Muthukumar A … +7 more , Chandrasekar LB, Gnaneswari MD, Karunakaran M, Balakrishnan T, Shunmuga Sundaram P, Thirumalai J, Shanmugapriya D
Biochem Biophys Res Commun · 2026 Aug · PMID 42284992 · Publisher ↗
Novel PrSmZnO nanoparticles are prepared by the chemical precipitation method. The doping concentrations of praseodymium and samarium are selected to be equal, with values established at 0, 1, 3, and 5%. The crystallite...
Novel PrSmZnO nanoparticles are prepared by the chemical precipitation method. The doping concentrations of praseodymium and samarium are selected to be equal, with values established at 0, 1, 3, and 5%. The crystallite size, strain and lattice constants are examined from the XRD data. The prepared nanoparticles show a higher band gap of 3.654 eV when the doping concentration is set at 5%. The electron and hole concentration is in the order of 10-10/m The refractive index of the prepared materials is examined as a function of the doping concentration. The quenching is observed in the photoluminescence spectrum when the doping is done. The nanoparticles exhibit remarkable antibacterial efficacy against the bacterial strains considered in this work. Furthermore, the anticancer properties of both undoped and doped nanoparticles are meticulously examined against the human breast cancer cell line. The ZnO nanoparticles exhibited 90% inhibition of breast cancer cell proliferation, whereas 5% Pr, Sm dual-doped ZnO nanoparticles showed 94% inhibition at 30 μg/mL. The IC50 value has been significantly (P<0.05) reduced from 10.72 ± 0.05 to 9.1 ± 0.05 μg/mL upon doping proves the potential of Pr, Sm dual-doped ZnO nanoparticles as an anticancer agent. The degradation of methylene blue under visible light is explored. The degradation efficiency, reusability, and kinetic rate constants are analyzed.
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