European Journal Of Histochemistry[JOURNAL]
Sun
200 papers
Folic acid promotes autophagy to relieve metabolism-associated fatty liver disease by regulating NRF2.
Wen Y, Luo J, Shi C … +1 more , Wu J
Eur J Histochem · 2025 Sep · PMID 41186492 · Full text
Metabolism-associated fatty liver disease (MAFLD) is a liver disease characterized by hepatic steatosis and excessive accumulation of lipids, with a high global incidence, especially in populations with obesity, diabetes...
Metabolism-associated fatty liver disease (MAFLD) is a liver disease characterized by hepatic steatosis and excessive accumulation of lipids, with a high global incidence, especially in populations with obesity, diabetes and metabolic syndrome (MetS). As an important B vitamin, folate (FA) is stored mainly in the liver where it regulates oxidative stress, chronic inflammation and lipid metabolism. However, its regulatory role and mechanism of action in MAFLD are still poorly understood. Therefore, this study was conducted to investigate the regulatory effect of FA on MAFLD. The MAFLD rat model was induced by a high-fat diet (HFD), and HepG2 cells were treated with 0.3 mM palmitic acid (PA) for 24 h to establish a cell model. The expression of relevant genes and proteins was detected by RT-qPCR and Western blotting. Injury to HepG2 cells and rat liver tissues was evaluated via hematoxylin and eosin staining, Oil red O staining, ELISA and CCK-8 assay. FA treatment inhibited body weight gain in rats and reduced the levels of liver injury indicators (aspartate and alanine aminotransferase, and Alkaline phosphatase), blood lipids (total cholesterol, triglycerides and free fatty acids) and inflammatory cytokines (TNF-α, IL-6, and IL-1β), reducing lipid accumulation and pathological damage in the liver and ultimately alleviating the progression of MAFLD. Moreover, FA treatment promoted the expression of the autophagy-related protein LC3 II/I, inhibited the expression of p62, and increased the formation of autophagosomes, thereby alleviating PA-induced damage to HepG2 cells. Furthermore, NRF2 expression is downregulated in MAFLD and can be upregulated by FA treatment. Further examination revealed that knocking down NRF2 could partially attenuate the inhibitory effect of FA on PA-induced HepG2 cell injury. In conclusion, FA activates autophagy by promoting the expression of NRF2, thereby alleviating the development of MAFLD.
Immunohistochemical analysis of YB-1 expression in the developing mouse eye.
Nass AF, Wolf H, Sel S … +2 more , Kalinski T, Nass N
Eur J Histochem · 2025 Sep · PMID 41186489 · Full text
Cold shock domain (CSD) proteins, such as YB-1, play a crucial role in the regulation of transcription, mRNA stability, and translation. Consequently, YB-1 is implicated in processes such as cell differentiation, oncogen...
Cold shock domain (CSD) proteins, such as YB-1, play a crucial role in the regulation of transcription, mRNA stability, and translation. Consequently, YB-1 is implicated in processes such as cell differentiation, oncogenesis and oxidative stress response. The development of the eye is a complex process that involves the differentiation of numerous highly specialized cell types. We hypothesized that YB-1 is involved in both eye development and stress defense mechanisms. As an initial step, we investigated the expression of YB-1 during the embryology of the mouse eye. YB-1 mRNA could be detected by RT-PCR and sequencing the PCR product in retinal tissue of adult mice. To elucidate the expression pattern of YB-1 protein during mouse eye development, we analyzed its expression in the developing mouse eye at embryonic day 13 (E13), E15, E18 and postnatal day 14 (P14) using immunohistochemistry. Expression of the YB-1 protein was detected in all retinal cells, as well as in the corneal and lens epithelial cells, throughout all stages of eye development examined. These findings suggest that YB-1 could have a significant role in the eye, potentially related to development and differentiation.
Vagal afferent projections from the pharyngeal jaw of the cichlid Nile tilapia ().
Imura K, Takeda A, Endo M … +2 more , Nasu M, Funakoshi K
Eur J Histochem · 2025 Sep · PMID 41117017 · Full text
We identified vagal innervation in the pharyngeal tooth and jawbones of Nile tilapia through macroscopic observations and immunohistochemistry. We also revealed the apposition of the nerve and osteoclasts in the pharynge...
We identified vagal innervation in the pharyngeal tooth and jawbones of Nile tilapia through macroscopic observations and immunohistochemistry. We also revealed the apposition of the nerve and osteoclasts in the pharyngeal jaw, suggesting the possibility of neuronal regulation for bone remodeling. However, the central projection from the vagal nerve, which innervates the pharyngeal jaws, remains unknown. To determine the projection of the vagus nerve in the brain, we applied carbocyanine dye (DiI) into the vagus nerve, revealing DiI-labeled neurons in the caudal vagal ganglion. The labeled fibers of the neurons were then traced to the vagal lobe, revealing that they branched and ran dorsally before terminating in a band-like pattern. Meanwhile, the labeled fibers running ventral to the vagal lobe were directed toward the dorsal motor nucleus of the vagus and did not have a definite terminal structure. The vagus nerve innervates the pharyngeal jaw, mainly projects to the vagal lobe, where it receives gustatory information. Pharyngeal tooth-derived sensory information might occur during occlusion and be processed precisely for determining the regurgitation and swallowing of prey.
Maresin 1 alleviates myocardial ischemia-reperfusion injury in rats by suppressing inflammation.
Xiao H, Liu J, Cai Q … +3 more , Liang S, Hu Z, Chen X
Eur J Histochem · 2025 Sep · PMID 41081431 · Full text
Myocardial ischemia-reperfusion injury (MIRI) induces severe inflammatory damage to cardiac tissue, leading to structural impairment and functional decline. Maresin 1 (MaR1) is an anti-inflammatory lipid mediator derived...
Myocardial ischemia-reperfusion injury (MIRI) induces severe inflammatory damage to cardiac tissue, leading to structural impairment and functional decline. Maresin 1 (MaR1) is an anti-inflammatory lipid mediator derived from macrophages that has shown protective effects in various inflammatory conditions. This study investigated the anti-inflammatory properties and underlying mechanisms of MaR1 in the context of MIRI, both in vivo and in vitro. A rat model of MIRI was established, and MaR1 was administered subcutaneously once daily for one week prior to model induction. Cardiac function was monitored intraoperatively, and serum and myocardial tissue samples were collected postoperatively for analysis. Structural alterations, myocardial injury biomarkers, and inflammatory cytokines were evaluated. In vitro experiments using H9c2 rat cardiomyocytes assessed the effects of MaR1 on cell viability and proliferation. MaR1 treatment significantly improved cardiac function impaired by MIRI, preserved myocardial architecture, and reduced serum and tissue levels of creatine kinase, lactate dehydrogenase, cardiac troponin I, and pro-inflammatory cytokines (IL-1β, IL-6, IL-8, MCP1, and TNF-α). In contrast, MaR1 enhanced the expression of the anti-inflammatory cytokine IL-10. In cultured cardiomyocytes, MaR1 promoted viability and proliferation. Collectively, these findings demonstrate that MaR1 confers protection against MIRI by attenuating inflammation, preserving myocardial structure, improving cardiac function, and enhancing cardiomyocyte survival, underscoring its potential as a therapeutic agent for ischemic cardiac injury.
Erratum - Localization of ανβ6 integrin-TGF-β1/Smad3, mTOR and PPARγ in experimental colorectal fibrosis.
Latella G, Vetuschi A, Sferra R … +2 more , Speca S, Gaudio E
Eur J Histochem · 2025 Sep · PMID 41081420 · Full text
This corrects the article published in the European Journal of Histochemistry 2013;57:e40.
This corrects the article published in the European Journal of Histochemistry 2013;57:e40.
Guilu Erxian oral liquid mitigates oxidative damage in spermatogonial cells miR-6739-5p modulation and PI3K/AKT pathway activation: a functional histocytochemical study.
Sun Z, Fan X, Liu Z
Eur J Histochem · 2025 Sep · PMID 41036671 · Full text
Oxidative stress is a major contributor to male infertility, particularly oligoasthenozoospermia. This study aimed to investigate the cytoprotective mechanism of Guilu Erxian Oral Liquid (GLEX) against H₂O₂-induced oxida...
Oxidative stress is a major contributor to male infertility, particularly oligoasthenozoospermia. This study aimed to investigate the cytoprotective mechanism of Guilu Erxian Oral Liquid (GLEX) against H₂O₂-induced oxidative damage in spermatogonial cells, focusing on miR-6739-5p regulation and activation of the PI3K/AKT pathway using histocytochemical approaches. An oxidative stress model was established in rat spermatogonial stem cells (SSCs) with 250 µM H₂O₂. Cell proliferation, apoptosis, reactive oxygen species (ROS) accumulation, and DNA oxidative damage were assessed using EdU incorporation, flow cytometry, immunofluorescence, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) ELISA. Expression of miR-6739-5p and Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) pathway components (PIK3CA, p-PI3K, p-AKT) was evaluated by RT-qPCR and Western blotting. The interaction between miR-6739-5p and PIK3CA was confirmed via dual-luciferase reporter assay. The cytoprotective effects of GLEX were examined through pre-treatment and quantified using histochemical and cytological markers. H₂O₂ treatment significantly impaired cell viability, increased apoptosis and ROS production, and upregulated miR-6739-5p. Overexpression of miR-6739-5p exacerbated damage, while silencing reversed it and restored PI3K/AKT signaling. GLEX pretreatment effectively reduced miR-6739-5p expression, restored cell viability, suppressed oxidative and inflammatory markers (ROS, 8-OHdG, TNF-α, IL-1β), and enhanced PI3K/AKT activation. These effects were comparable to PI3K pathway activation. GLEX confers histocytochemical protection to spermatogonial cells under oxidative stress by downregulating miR-6739-5p and activating the PI3K/AKT pathway. This study highlights a novel regulatory mechanism and supports GLEX as a potential therapeutic agent for oxidative stress-associated male infertility.
miR-129-5p regulates HMGB1/RAGE axis to inhibit pyroptosis and ameliorate cervical epithelial cell deterioration.
Wang H, Sidike D, Liu P … +2 more , Suo L, Niyazi H
Eur J Histochem · 2025 Sep · PMID 40985579 · Full text
Cervical cancer is a serious gynecological malignancy, and the specific mechanisms of miR-129-5p remain unclear. This study aims to investigate the mechanism by which miR-129-5p regulates the high mobility group box 1 (H...
Cervical cancer is a serious gynecological malignancy, and the specific mechanisms of miR-129-5p remain unclear. This study aims to investigate the mechanism by which miR-129-5p regulates the high mobility group box 1 (HMGB1/receptor for advanced glycation end-products (RAGE) axis to inhibit pyroptosis and ameliorate cervical epithelial cell deterioration. Using RT-qPCR and Western blotting, we detected significantly downregulated miR-129-5p and upregulated HMGB1 in cervical cancer cells. To establish a deterioration model, we stimulated cervical epithelial cells with lipopolysaccharide (LPS). Further results revealed that miR-129-5p overexpression markedly reduced HMGB1 expression, suppressed RAGE activation, and decreased pyroptosis executer GSDMD-N production. Additionally, we conducted miR-129-5p overexpression and knockdown experiments to verify its regulatory effects on the HMGB1/RAGE axis and downstream pathways. Caspase-1 activity assays confirmed reduced pyroptosis upon miR-129-5p overexpression. Cell viability and proliferation were assessed using EdU incorporation assays and colony formation experiments. Our data demonstrated significant downregulation of miR-129-5p in cervical cancer cells. Overexpression of miR-129-5p substantially reduced HMGB1 expression and inhibited RAGE activation, thereby decreasing production of the pyroptosis executer GSDMD-N. LPS stimulation potently activated the HMGB1/RAGE axis and induced pyroptosis, while miR-129-5p overexpression inhibited these processes and ameliorated in vitro cervical epithelial cell deterioration. Cells overexpressing miR-129-5p exhibited attenuated caspase-1 activity with enhanced survival and proliferation following LPS treatment. Collectively, these in vitro findings indicate that miR-129-5p suppresses HMGB1/RAGE-mediated pyroptosis and cellular deterioration and also provide new mechanistic insights for cervical cancer therapeutics.
miR-199a-5p inhibited HIF-1α to suppress the proliferation, migration, and differentiation of cardiac stem cells.
Li S, Zhang C, Liu Y … +3 more , Meng C, Xie Y, Li S
Eur J Histochem · 2025 Sep · PMID 40984793 · Full text
The cardiac stem cells (CSCs) are essential in improving myocardial infarction (MI). Although miR-199a-5p and hypoxia-inducible factor-1 alpha (HIF-1α) were proven to participate in the process of heart repair, the relat...
The cardiac stem cells (CSCs) are essential in improving myocardial infarction (MI). Although miR-199a-5p and hypoxia-inducible factor-1 alpha (HIF-1α) were proven to participate in the process of heart repair, the related mechanisms are still unclear. This study aimed to explore the effects of miR-199a-5p and HIF-1α on c-kit+ cells and their regulatory mechanisms. After isolating, purifying, and identifying CSCs (c-kit+ cells) from mice, they were subjected to a hypoxia model. After the c-kit+ cells were transfected with corresponding transfectants, the CCK-8, EdU staining, and wound healing approaches were used to evaluate their cell viability, proliferation, and migration. The targeted relation between miR-199a-5p and HIF-1α was determined using a dual-luciferase reporter. Immunofluorescence staining, RT-qPCR, and Western blot approaches were employed to determine Nkx2.5, CD31, α-SMA, miR-199a-5p, and HIF-1α expression. Overexpressing miR-199a-5p and knocking down HIF-1α both inhibited the cell viability (p<0.01), reduced the proliferation (p<0.05), suppressed the migration (p<0.001), and down-regulated the Nkx2.5, CD31, and α-SMA expression of c-kit+ cells (p<0.05). Overexpressing HIF-1α effectively reversed the effects of overexpressing miR-199a-5p on c-kit+ cells (p<0.05). Taken together, miR-199a-5p negatively targeted HIF-1α to inhibit the proliferation, migration, and differentiation of c-kit+ cells.
Expression of nestin, parvalbumin and otoferlin during cochlear development in the mouse: an immunofluorescence study.
Liu W, Zhang Y, Liang C … +1 more , Yang S
Eur J Histochem · 2025 Sep · PMID 40984791 · Full text
To elucidate the proteins associated with cochlear development and auditory formation from a histomorphological point of view, this study examined the spatio-temporal expression pattern of nestin, parvalbumin, and otofer...
To elucidate the proteins associated with cochlear development and auditory formation from a histomorphological point of view, this study examined the spatio-temporal expression pattern of nestin, parvalbumin, and otoferlin in the mouse cochlea from embryonic day 17 (E17) to postnatal day 28 (P28) using immunofluorescence. Our findings revealed that nestin was broadly expressed in developing otic mesenchyme cells beneath the basilar membrane, medial to the greater epithelial ridge, and adjacent to the developing stria vascularis during late embryonic stages (E17 and E18.5). From P1 to the onset of hearing (P14), nestin was primarily expressed in fibrocytes derived from otic mesenchyme cells in the spiral ligament and spiral limbus, as well as in tympanic border cells. Dual immunofluorescence staining of nestin with Isolectin B4 (IB4), a specific vascular endothelial marker, showed the location of nestin in the blood vessels within the cochlear lateral wall. Notably, in adults (P28), nestin expression was downregulated in the fibrocytes of the spiral ligament and spiral limbus but persisted in the tympanic border cells. Parvalbumin immunolabeling was consistently observed in spiral ganglion neurons (SGNs) and inner hair cells (IHCs) from E17 through adulthood. By P1, parvalbumin expression extended to all three rows of outer hair cells (OHCs) and persisted into adulthood. Transient parvalbumin expression was also noted in afferent nerve fibers innervating the IHCs during early postnatal stages. Otoferlin labeling was predominantly detected in the cytoplasm of IHCs, with limited temporal expression in OHCs from P6 to P10. Taken together, these results illustrated the dynamic expression of nestin, parvalbumin and otoferlin during cochlear development and suggested their important function in cochlear development.
Effects of Notch signaling on proliferation, angiogenesis, and adipogenesis of hemangioma-derived stem cells.
Wang W, Chen S, Wang Y … +2 more , Jie C, Shen W
Eur J Histochem · 2025 Jun · PMID 40888512 · Full text
Hemangioma-derived stem cells (Hem-SCs) constitute the cellular basis for adipogenesis during infantile hemangioma (IH) regression, with Notch signaling implicated in this process. To elucidate Notch's role in Hem-SCs bi...
Hemangioma-derived stem cells (Hem-SCs) constitute the cellular basis for adipogenesis during infantile hemangioma (IH) regression, with Notch signaling implicated in this process. To elucidate Notch's role in Hem-SCs biology, we isolated primary Hem-SCs from proliferative-phase IH specimens and validated their stem cell characteristics. Three days post-intervention with the γ-secretase inhibitor DAPT (N‑[N‑(3,5‑difluorophenacetyl)‑L‑alanyl]‑S‑phenylglycine t‑butylester), we assessed Notch and PI3K/AKT signaling dynamics while concurrently measuring vascular endothelial growth factor receptor (VEGFR) protein expression. Cellular proliferation was quantified via CCK-8 assay. During adipogenic differentiation (Day 14), RTqPCR evaluated Notch pathway genes (Notch1, Jagged1, Hes1), while adipogenic commitment was determined through Oil Red O staining and adipocyte-specific gene expression (PPARγ, C/EBPα). We demonstrate that DAPT suppresses Notch and PI3K/AKT signaling in Hem-SCs, concomitantly enhancing cellular proliferation and angiogenesis. Simultaneous analysis of VEGFR expression revealed differential DAPT-mediated regulation: VEGFR1 downregulation with concomitant VEGFR2 upregulation. During adipogenic induction, Notch pathway genes (Notch1, Jagged1, Hes1) were significantly downregulated. DAPT treatment further elevated adipogenic markers (PPARγ, C/EBPα) and lipid accumulation. Crucially, co-administration of the PI3K activator 740Y-P reversed DAPT-induced adipogenesis. Mechanistically, Notch inhibition promotes Hem-SCs proliferation, angiogenesis, and adipocyte differentiation by attenuating PI3K/AKT signaling.
Solamargine inhibited the progression of non-small cell lung cancer by activating T cells.
Zhang C, Sun Y, Jiang W … +3 more , Wu L, Fang Q, Wang Q
Eur J Histochem · 2025 Jun · PMID 40888491 · Full text
Lung cancer is the leading cause of cancer-related death globally and the most common cancer type. Solamargine is an extract from the traditional Chinese medicine, Long Kui, which exhibits antitumor effects in a number o...
Lung cancer is the leading cause of cancer-related death globally and the most common cancer type. Solamargine is an extract from the traditional Chinese medicine, Long Kui, which exhibits antitumor effects in a number of cancer types, including lung cancer. However, the possible association between solamargine and the tumor microenvironment (TME) in non-small cell lung cancer (NSCLC) remains to be elucidated. In the present study, Cell Counting Kit-8 and 5-Ethynyl-2'-deoxyuridine (EdU) assays were used to evaluate the viability and proliferation of NSCLC cells, respectively. In addition, NSCLC cells were co-cultured with peripheral blood mononuclear cells with or without prior solamargine treatment to evaluate the possible association between solamargine and the TME. The results indicated that solamargine can inhibit NSCLC cell proliferation and migration directly. In addition, it was demonstrated that solamargine can prevent the progression of NSCLC indirectly via activating the function of T cells. These findings may provide a novel theoretical basis in drug discovery for the treatment of NSCLC.
circRNA-79530 regulates Twist-mediated mitochondrial damage ponging miR-214 affecting hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes.
Yu Z, Xu W, Teng Y … +6 more , Li T, Guo R, Li J, Li X, Li Y, Hao Y
Eur J Histochem · 2025 Jun · PMID 40844089 · Full text
Cardiomyocyte injury related to hypoxia/reoxygenation (H/R) is pivotal in myocardial infarction. The circular RNA circRNA-79530 (circ79530) may play a regulatory role in this process, though its exact function has yet to...
Cardiomyocyte injury related to hypoxia/reoxygenation (H/R) is pivotal in myocardial infarction. The circular RNA circRNA-79530 (circ79530) may play a regulatory role in this process, though its exact function has yet to be elucidated. This research explores the role of circRNA-79530 in H9c2 cells under H/R, with a particular focus on its interactions with miR-214 and the transcription factor Twist. It also examines their subsequent effects on mitochondrial function and oxidative stress. H9c2 cardiomyocytes were subjected to H/R to model myocardial injury. We measured circRNA-79530, miR-214, and Twist levels via RT-qPCR, with Twist protein via Western blotting. ROS levels were quantified using DCFH-DA, and cell viability and injuries were assessed through CCK-8, LDH, SOD, and MDA assays, respectively. Mitochondrial performance was assessed through various methods, including the measurement of mitochondrial membrane potential using JC-1 staining, the quantification of ATP levels, and the examination of the protein levels of mitochondrial complexes, as well as the expression of fusion proteins. Our findings indicated that downregulation of circRNA-79530 modulated miR-214 and Twist expression, influencing mitochondrial dynamics and ROS production. Knockdown of circRNA-79530 improved cell viability, reduced oxidative stress and enhanced mitochondrial function. Additionally, overexpression of miR-214 mitigated Twist expression, further supporting the effect of miR-214 in H/R conditions. circRNA-79530 could worsen oxidative stress and mitochondrial dysfunction, and regulate Twist-mediated mitochondrial damage via sponging miR-214 in H9c2 cells under H/R conditions.
Expression of bone morphogenetic protein signaling pathway players in the jejunum and colon of adult rats.
Cogo E, Fouché E, Buisson C … +4 more , Omotoyinbo A, Pierre F, Guéraud F, Plaisancié P
Eur J Histochem · 2025 Jun · PMID 40836864 · Full text
The bone morphogenetic protein (BMP) pathway, which plays a crucial role in the control of intestinal epithelial cell homeostasis, has been studied in mice and humans, leading to an understanding of its involvement in se...
The bone morphogenetic protein (BMP) pathway, which plays a crucial role in the control of intestinal epithelial cell homeostasis, has been studied in mice and humans, leading to an understanding of its involvement in several intestinal pathologies. However, the expression and localization of the various actors (ligands, antagonists, receptors) of this pathway remain unknown in the rat intestine, although this species is widely used in pathophysiology studies. Here, we aimed to determine the expression and localization of the various players in the BMP pathway in the jejunum and colon of the rat using RT-qPCR and immunohistochemistry. BMP2, mainly localized in epithelial cells, was the most expressed ligand in the jejunum and colon in comparison with BMP4, BMP6 and BMP7. We showed for the first time that BMP7 was highly expressed in epithelial cells in both tissues. BMP2, BMP6 and BMP7 ligands were also present in the enteric nervous plexuses, as the BMP receptors and antagonists Noggin and Chordin-like 1. The expression of BMP antagonists and ligands in enterocytes and mature colonocytes could suggest a paracrine or autocrine feedback modulation at the cellular level. Finally, all the studied BMP actors were present in colonic vessel walls including GREM1, a BMP antagonist described as pro-angiogenic and also being a ligand for VEGFR receptors. These data provided a good correlation between the observations in rats compared to those in humans and highlighted the importance of the BMP pathway not only in the intestinal epithelium, but also in both the enteric nervous system and vascular system. Our work lays the foundations for further studies on the involvement of the BMP pathway in rat models of intestinal pathophysiology.
Aloe-emodin ameliorates chronic kidney disease fibrosis by inhibiting PI3K-mediated signaling pathway.
Chen M, Zhu W, Chen Y … +5 more , Shang J, Wang W, Yan X, Liu P, Zhou Y
Eur J Histochem · 2025 Jun · PMID 40832995 · Full text
Chronic kidney disease (CKD) impacts a vast number of individuals worldwide, culminating in renal fibrosis. Renal fibrosis serves as the main reason for end-stage renal failure. However, the current targeted treatment me...
Chronic kidney disease (CKD) impacts a vast number of individuals worldwide, culminating in renal fibrosis. Renal fibrosis serves as the main reason for end-stage renal failure. However, the current targeted treatment methods for renal fibrosis remain scarce. Aloe-emodin (AE) is a naturally occurring compound discovered in rhubarb and aloe. In this research, we investigated the underlying mechanisms of AE in adenine-induced mouse renal fibrosis models and TGFβ-1 stimulated renal tubular epithelial cells (HK-2). It was discovered that AE not only decelerated the decline of renal function in adenine-treated mice but also suppressed the expression of Collagen I and Fibronectin. Furthermore, network pharmacology analysis suggested that AE's treatment of renal fibrosis might function via the PI3K/Akt/GSK3β signaling pathway. In vivo and in vitro Western blot and immunofluorescence findings demonstrate that AE significantly resists the advancement of renal fibrosis by inhibiting α-smooth muscle actin (α-SMA) and vimentin. Simultaneously, findings from 740Y-P (a PI3K agonist) and siRNA (PI3K) indicate that AE inhibits the expression of the PI3K/Akt/GSK3β cascade by lowering PI3K's phosphorylation level. From a mechanistic perspective, through molecular docking and plasmid transfection, the specific base sequence of PI3K in HK-2 cells was altered for experimental validation. The outcomes illustrate that AE can directly bind with PI3K, inhibiting its activation, impeding the PI3K/Akt/GSK3β signal transmission, thereby ultimately suppressing renal fibrosis progression. In conclusion, PI3K/Akt/GSK3β is a potential therapeutic target for CKD-related renal fibrosis, making AE a promising new treatment alternative for this condition.
Forever particles: histochemistry in the plasticene age.
Camia B, Casasco A, Monti M
Eur J Histochem · 2025 Jun · PMID 40832994 · Full text
The statement "Plastics define the way we live today" summarizes the findings of the Plastic Europe 2020 final document (https://plasticseurope.org/knowledge-hub/plastics-the-facts-2020/). Sadly, this also means that the...
The statement "Plastics define the way we live today" summarizes the findings of the Plastic Europe 2020 final document (https://plasticseurope.org/knowledge-hub/plastics-the-facts-2020/). Sadly, this also means that the plastic waste generated over the next decade is likely to become unmanageable. By 2050, plastic usage is expected to triple, resulting in a similar increase in plastic waste, with approximately half of it ending up in landfills. Emerging research indicates that micro and nanoplastics have been found in various human organs, including the gonads, placenta, blood, arteries, lungs, liver, kidney, and even the brain. This raises significant questions about their pervasive presence within our bodies and their potential threat to health. In addition to their harmful effects, these "forever particles" (micro/nanoplastics) can serve as Trojan horses, transporting additional pollutants such as bacteria and heavy metals into our bodies. In this review, we explore key aspects of the plastics crisis and urge the scientific community -especially those in the fields of cytochemistry and histochemistry, which adeptly connect morphology with function- to investigate the harmful effects of micro and nanoplastics that we encounter daily through ingestion or inhalation. This research should focus on various physiological levels, including DNA, cells, and tissues.
Histological and histochemical characterization of the musk gland in forest musk deer (): a preliminary study.
Wang Q, Han C, Zhang D … +4 more , Liu Y, Gao Y, Zhang H, Hu D
Eur J Histochem · 2025 Jun · PMID 40637047 · Full text
Musk is a biologically valuable secretion from the musk gland of male musk deer, with significant economic and medicinal importance. Due to severe decline and depletion of wild musk deer population, captive breeding of m...
Musk is a biologically valuable secretion from the musk gland of male musk deer, with significant economic and medicinal importance. Due to severe decline and depletion of wild musk deer population, captive breeding of musk deer has become the primary approach for sustainable musk production. So far, the histological structure and secretion mechanism of the musk gland remain incompletely understood. In this study, we employed histological and immunohistochemical (IHC) techniques, along with three-dimensional (3D) tissue reconstruction, to systematically analyze the cellular composition and secretory functions of the musk gland in forest musk deer (Moschus berezovskii). Our results revealed that the musk gland was primarily composed of acinar structures containing two distinct glandular cell (GC) types based on the histological observation. IHC results showed type I glandular cells (GCIs) predominantly expressed GALNT7 while type II glandular cells (GCIIs) mainly expressed BMP6. The 3D reconstruction demonstrated structural heterogeneity along the gland's longitudinal axis, with the proportion of the acinar area varying between 40% and 65%. This is the first time that a detailed 3D view of musk gland in forest musk deer has been shown, which provides essential histological insights into musk gland function in this species. These preliminary observations may provide useful groundwork for future investigations into the regulatory mechanisms of musk secretion.
NR4A3 suppresses bladder cancer progression by modulating autophagy the PI3K/AKT/mTOR pathway.
Fan L, Xu F, Liu S … +6 more , Wu D, Wang S, Pan X, Zhou Y, Qu L, Zhou W
Eur J Histochem · 2025 Jun · PMID 40586548 · Full text
Bladder cancer (BC) is a prevalent and aggressive malignancy with high recurrence. Autophagy plays a dual role in cancer, acting as a tumor suppressor early on and promoting survival in later stages. NR4A3, a nuclear rec...
Bladder cancer (BC) is a prevalent and aggressive malignancy with high recurrence. Autophagy plays a dual role in cancer, acting as a tumor suppressor early on and promoting survival in later stages. NR4A3, a nuclear receptor with tumor-suppressive effects in other cancers, has not been explored in BC. NR4A3 expression was analyzed using TCGA data and validated in clinical BC samples via immunohistochemistry and RT-qPCR. NR4A3-overexpressing BC cell lines (5637, T24) were created using lentiviral vectors. Cell viability, proliferation, migration, and invasion were assessed through CCK-8, EdU, and Transwell assays. Autophagy was measured by microtubule-associated protein 1A/1B-light chain 3 (LC3), autophagy-related protein 5 (ATG5), Beclin-1 and p62 expression via immunofluorescence and Western blotting. The phosphoinositide 3-kinase (PI3K) / protein kinase B (AKT) / mammalian target of rapamycin (mTOR) pathway was examined by assessing phosphorylation levels. It was found that NR4A3 was significantly downregulated in BC tissues. Overexpression of NR4A3 inhibited BC cell proliferation, migration, and invasion, while promoting apoptosis. NR4A3 overexpression increased autophagy markers and suppressed PI3K/AKT/mTOR signaling. Autophagy inhibition reversed these effects. In conclusion, NR4A3 suppresses BC progression by promoting autophagy via the PI3K/AKT/mTOR pathway. Targeting NR4A3-mediated autophagy may provide a novel therapeutic strategy for BC.
Targeting EphA2 suppresses the proliferation, migration and invasion of endometriosis the AMPK signaling pathway.
Yang C, Wang S, Li M … +2 more , Pang X, Tan A
Eur J Histochem · 2025 Jun · PMID 40525819 · Full text
Endometriosis is a benign disease with similar characteristics to tumors. Recent studies have found that the erythropoietin-producing hepatoma receptor A2 (EphA2) has the dual effect of promoting tumor and inhibiting tum...
Endometriosis is a benign disease with similar characteristics to tumors. Recent studies have found that the erythropoietin-producing hepatoma receptor A2 (EphA2) has the dual effect of promoting tumor and inhibiting tumor. The objective of this study was to explore the specific regulatory mechanism of EphA2 in endometriosis. The expression level of Eph protein family in endometriosis was analyzed by bioinformatics method. At the clinical level, qPCR, Western blot and immunohistochemistry were used to verify the correlation between increased EphA2 levels and endometriosis. The effects of blocking EphA2 on cell migration, invasion, proliferation and apoptosis of primary eutopic endometriotic stromal cells were explored in vitro. Our study indicated that EphA2 expression was elevated in endometriosis patients, and blocking EphA2 in vitro inhibited cell proliferation, migration and invasion through AMPK signaling pathway. Targeting EphA2 can inhibit the progression of endometriosis through the AMPK signaling pathway.
Tanshinone IIA attenuates hepatic stellate cell activation, oxidative stress, and liver fibrosis by inhibiting YAP signaling.
Wang D, Tan Q, Zheng Q … +2 more , Ma Y, Feng L
Eur J Histochem · 2025 Jun · PMID 40525818 · Full text
Tanshinone IIA is derived from Salvia miltiorrhiza and has multiple therapeutic targets and functions. The exact therapeutic effects on liver fibrosis as well as the underlying hepatoprotective mechanisms are still lacki...
Tanshinone IIA is derived from Salvia miltiorrhiza and has multiple therapeutic targets and functions. The exact therapeutic effects on liver fibrosis as well as the underlying hepatoprotective mechanisms are still lacking. A liver fibrosis model was established via ligation of the common bile duct ligation (BDL). The mice were intraperitoneally administered different concentrations of tanshinone IIA (4 mg/kg, 8 mg/kg) for 2 weeks. Liver function was assessed through hematoxylin and eosin and Sirus red staining. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), glutathione (GSH) and malondialdehyde (MDA) were quantified by enzyme-linked immunosorbent assay (ELISA), via microplate reader. The total iron content of the liver was quantified via Triple Quad-ICP-MS. TGFβ-induced hepatic stellate cells (HSCs), a cell model of liver fibrosis, were treated with tanshinone IIA at different concentrations (10 mM, 20 mM, 30 mM, 40 mM). The combination of tanshinone IIA with YAP agonists was applied in activated HSCs and animal models. Tanshinone IIA treatment relieved BDL-induced liver fibrosis; mitigated histological liver damage; lowered the serum ALT and AST levels; reduced macrophage infiltration and the MDA and iron contents; and increased the GSH and GPX4 levels by inhibiting YAP signaling. tanshinone IIA also suppressed the activation of HSCs and collagen production through blocking the YAP signaling pathway. The YAP agonist reversed the therapeutic effect of tanshinone IIA on activated HSCs and BDL-induced liver fibrosis. Tanshinone IIA inhibited HSC activation and oxidative stress and alleviated liver fibrosis by inhibiting the YAP signaling pathway.
Proceedings of the 34th National Conference of the Italian Group for the Study of Neuromorphology "Gruppo Italiano per lo Studio della Neuromorfologia" G.I.S.N.
Velia D'Agata CC
Eur J Histochem · 2024 Nov · PMID 40488585 · Publisher ↗
Proceedings of the 34th National Conference of the Italian Group for the Study of Neuromorphology "Gruppo Italiano per lo Studio della Neuromorfologia" G.I.S.N., Catania, November 22-23, 2024.
Proceedings of the 34th National Conference of the Italian Group for the Study of Neuromorphology "Gruppo Italiano per lo Studio della Neuromorfologia" G.I.S.N., Catania, November 22-23, 2024.
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