Alzheimer's disease (AD) is associated with hyperglycaemia and amyloid beta (Aβ) accumulation. In the present study, we investigated whether an aqueous extract of Lam. (CCWE) improved cognitive disorder in a hyperglycae...Alzheimer's disease (AD) is associated with hyperglycaemia and amyloid beta (Aβ) accumulation. In the present study, we investigated whether an aqueous extract of Lam. (CCWE) improved cognitive disorder in a hyperglycaemic and cognitive-impaired mouse model. Hyperglycaemia was induced by streptozotocin (STZ, 50 mg/kg) and a single intracerebroventricular injection of Aβ (25 nM) was performed. The Aβ-injected hyperglycaemic mice were then administered CCWE (100 or 200 mg/kg/day) for 14-d. The protective effects of the CCWE were evaluated by behavioural tests and western blot analysis. The bioactive compounds in CCWE were isolated by UPLC-QTOF/MS analysis. The administration of CCWE improved the learning and memory function in STZ/Aβ-injected mice. Moreover, CCWE positively regulated the amyloidogenic pathway-related proteins and insulin signalling-related proteins. The bioactive components in CCWE were also identified. These findings suggest the possibility of CCWE as a potential candidate for the dual-targeting treatment of hyperglycaemia and AD.
The consumption of açaí has been shown to be beneficial to health. This study aimed to evaluate the effects of juçara açai (JU, ) administration before gestation on the biometric, metabolic, and oxidative status in pregn...The consumption of açaí has been shown to be beneficial to health. This study aimed to evaluate the effects of juçara açai (JU, ) administration before gestation on the biometric, metabolic, and oxidative status in pregnant rats of advanced maternal age. Healthy female Wistar rats were treated with JU pulp via gavage from postnatal day 168 to 210. After treatment, the rats were mated, and during the 20 days of pregnancy, they were evaluated for body weight (BW), glucose tolerance, adipose tissue and liver weight, the lipid profile, and hepatic oxidative status. At birth, the offspring were weighed and counted. It was observed that JU reduced just maternal glycaemia. The maternal preconceptional treatment did not affect offspring BW. These results suggest that JU could be a safe nutritional intervention during the preconception period in advanced maternal age.
CONTEXT: Cardiovascular diseases (CVDs) remain a leading global cause of mortality, necessitating non‑pharmacological interventions such as exercise. Meteorin‑like protein (Metrnl), an exercise‑induced myokine and adipok...CONTEXT: Cardiovascular diseases (CVDs) remain a leading global cause of mortality, necessitating non‑pharmacological interventions such as exercise. Meteorin‑like protein (Metrnl), an exercise‑induced myokine and adipokine, has emerged as a critical mediator of exercise‑mediated cardiovascular benefits, though its specific mechanisms and clinical implications remain underexplored. OBJECTIVE: This review synthesizes current evidence on Metrnl's role as a key exerkine in cardiovascular health, focusing on its exercise‑induced regulatory mechanisms, tissue‑specific effects, and therapeutic potential for CVD management. METHODS: A comprehensive analysis of preclinical and clinical studies was conducted, encompassing molecular, metabolic, and anti‑inflammatory pathways linked to Metrnl. Literature from PubMed, Scopus, and Web of Science was systematically reviewed to evaluate Metrnl's role in exercise‑mediated cardiovascular adaptations. RESULTS: Exercise‑induced Metrnl enhances endothelial function, vascular remodeling, and metabolic regulation via AMPK, PPARγ, and KIT receptor signaling. It promotes glucose/lipid metabolism, angiogenesis, and anti‑inflammatory responses, reducing atherosclerotic risks and improving cardiac repair post‑infarction. Clinically, Metrnl levels correlate with CVD severity, acting as a biomarker for risk stratification. Acute exercise elevates Metrnl, while chronic training effects vary by modality and population. Paradoxically, elevated plasma Metrnl in acute cardiac events predicts adverse outcomes, whereas reduced levels in chronic conditions (e.g., diabetes, heart failure) reflect metabolic dysregulation. DISCUSSION: Metrnl bridges exercise benefits to cardiovascular health through inter‑organ crosstalk, yet discrepancies exist in its chronic exercise‑mediated regulation. Its dual role as a protective mediator and stress‑responsive biomarker underscores context‑dependent interpretations. Unresolved questions include receptor specificity, tissue autonomy, and therapeutic delivery strategies. CONCLUSION: Metrnl is a pivotal exerkine with promising diagnostic and therapeutic potential for CVDs. Translating its exercise‑mediated benefits into clinical applications requires further human trials to validate mechanisms and optimize interventions. Harnessing Metrnl could revolutionize strategies for CVD prevention and rehabilitation, leveraging exercise's molecular advantages.
BACKGROUND: Behçet Disease (BD) is a chronic multi-systemic vasculitis of relapsing and remitting nature. Many recent studies have denoted the role of micro RNAs (MiRNAs) in the pathogenesis of BD. SUBJECTS AND METHODS:...BACKGROUND: Behçet Disease (BD) is a chronic multi-systemic vasculitis of relapsing and remitting nature. Many recent studies have denoted the role of micro RNAs (MiRNAs) in the pathogenesis of BD. SUBJECTS AND METHODS: Blood samples were withdrawn from 50 BD patients and 40 age and sex-matched healthy individuals in this study. RESULTS: Serum expression levels of miR-34a and miR-182 were significantly elevated in BD patients when compared to controls, < .001. However, serum expression levels of miR-378 were significantly decreased in BD patients compared to controls, < .001. miR-182 serum levels were also found to be elevated in active BD patients compared to patients in inactive state ( = .022). We found a significant association between miR-34 levels and joint affection in BD patients as well as a significant relation between miR-182 levels and each of neurological manifestations and genital ulcerations. In addition, a statistically significant positive correlations were proved in the current results between miR-182 expression and BDCAF score ( = 0.419, = .002) as well as severity score ( = 0.358, = .011). CONCLUSION: Our study denoted that the three miRNAs; miR-34a, miR-182, and miR-378 possibly play a crucial role in the pathogenesis of BD. The distinction of their serum levels between patients and healthy individuals suggested their potentiality as promising biomarkers for BD.
BACKGROUND: Any toxicity initially damages the hepatic system, followed by renal dysfunction. Previously, it was established that carbon tetrachloride (CCl) intoxication severely damaged hepatocytes. Moreover, CCl-mediat...BACKGROUND: Any toxicity initially damages the hepatic system, followed by renal dysfunction. Previously, it was established that carbon tetrachloride (CCl) intoxication severely damaged hepatocytes. Moreover, CCl-mediated toxicity significantly impacted immune functions and influenced the inflammatory response, with mitochondrial dysfunction. The present study focused on the levels of inflammatory markers and mitochondrial dysfunction, as well as the protective role of BHA and BHT. METHODS: In the present study, hepatorenal dysfunction was developed in experimental rats by applying a subcutaneous injection of CCl with a dose of 230 mg/kg bwt/rat/day. The level of immune toxicity was determined by measuring C-reactive protein (CRP), IL-6, 12, TNF-α, IL-10, and TGF-β in CCl4 intoxicated group and pretreated BHA and BHT groups. ROS generation and MMP were also measured in hepatic and renal cells using flow cytometric technique. RESULTS: The level of toxicity was determined by a significant increase of CRP (407.29%), IL-6 (525.65%), IL-12 (1026.54%), and TNF-α (1007.33%) in CCl intoxicated group, while IL-10 and TGF-β were significantly decreased 84.65% and 66.36%, respectively. CCl intoxication caused decreased mitochondrial membrane potential and high levels of intracellular ROS generation. Pretreatment with BHA (0.5 mg/kg/bwt) and BHT (0.8 mg/kg/bwt) significantly (<0.001, <0.05) reduced inflammatory markers in the CCl4-treated group, restored mitochondrial membrane potential and decreased intracellular ROS levels. CONCLUSION: BHA and BHT treatment could restrict the higher concentration of pro-inflammatory markers by scavenging ROS. Therefore, the study suggested that supplementation of BHA and BHT could be an alternative treatment for preventing hepatorenal dysfunctions.
BACKGROUND: Herbacetin, a flavonoid present in many types of herbs, which include linaceae, ephedraceae, and crassulaceae, exhibits a range of medicinal properties. 1-methyl-4-phenylpyridinium (MPP) is one of the neuroto...BACKGROUND: Herbacetin, a flavonoid present in many types of herbs, which include linaceae, ephedraceae, and crassulaceae, exhibits a range of medicinal properties. 1-methyl-4-phenylpyridinium (MPP) is one of the neurotoxins used in cell-based Parkinson's disease (PI) models. Whereas the precise chemical mechanism of iron association with free radical cell damage and apoptosis is yet unknown, intracellular irons are a key factor for MPP-derived apoptosis. METHODS: We examine whether the antiapoptotic properties of flaxseed bioflavonoid herbacetin (HB) are associated with the stimulation of the intrinsic caspase-dependent pathway and exposing of MPP caused neuronal death in the human dopaminergic neuroblastoma cells. Four groups were created out of the cells. Groups I, II, III, and IV are the control, HB+MPP, MPP, and HB, respectively. Following a 24-hour incubation period, the cells were subjected to several parameters. RESULTS: We discovered in neuroblastoma cells that HB dramatically reduced the cell death induced by MPP. Additionally, HB significantly reduced the formation of ROS and counteracted the reduction in MMP resulting from MPP treatment. HB reduces the stimulation of the intrinsic caspase-dependent apoptotic mechanism and suppresses the MPP-mediated apoptotic signalling pathway. Furthermore, HB predicted a better binding interaction with alpha-synuclein and drastically decreased alpha-synuclein expression and accumulation in neuroblastoma cells. CONCLUSION: Consequently, our findings imply that HB shields neurons by reducing oxidative stress, alpha-synuclein misfolding in neuroblastoma, and apoptosis prompts the death of neuroblastoma cells.
BACKGROUND: Hepatocellular carcinoma (HCC) is a major public health problem with increasing incidence and mortality worldwide. The methylenetetrahydrofolate reductase (MTHFR) 677 C > T polymorphism is associated with the...BACKGROUND: Hepatocellular carcinoma (HCC) is a major public health problem with increasing incidence and mortality worldwide. The methylenetetrahydrofolate reductase (MTHFR) 677 C > T polymorphism is associated with the development and progression of various tumours, while protein induced by vitamin K absence II (PIVKA-II) is an important tumour marker for the diagnosis of HCC. This study aims to investigate the relationship between the MTHFR 677 C > T polymorphism and serum PIVKA-II levels in HCC patients, providing new insights for early diagnosis, risk assessment, and prognosis evaluation of HCC. METHODS: This study included 120 HCC patients and 100 healthy controls. MTHFR 677 C > T genotyping was performed using fluorescent quantitative PCR, and serum PIVKA-II levels were measured. Bioinformatics analysis was used to explore the expression of the MTHFR gene in HCC and its relationship with prognosis. RESULTS: MTHFR 677 C > T TT carriers had an increased risk of HCC (OR = 2.393; 95% CI 1.055-5.429; = 0.037); the risk of HCC for T gene carriers was 58.3% higher than that for C gene carriers in the allele model (OR = 1.583; 95% CI 1.059-2.364; = 0.025). The difference in serum PIVKA-II concentration was statistically significant between the controls, stage I-II patients, and stage III-IV patients ( < 0.05), and the difference in serum PIVKA-II concentration was statistically significant between patients with the TT genotype and patients with the CC and CT genotypes (all values less than 0.05). UALCAN database analysis showed that MTHFR gene expression levels were increased in patients with HCC, and the high expression of the MTHFR gene was negatively correlated with patient survival rates. CONCLUSIONS: There is an association between the MTHFR 677 C > T TT genotype and serum PIVKA-II levels in HCC. This could help identify high-risk individuals and assess disease severity, providing a potential genetic biomarker for the diagnosis of HCC.
INTRODUCTION: Metabolic Syndrome (MetS) is a global health concern characterised by cardiometabolic risk factors, dysregulated adipokine signalling and inflammation. The study aimed to assess the serum levels of omentin...INTRODUCTION: Metabolic Syndrome (MetS) is a global health concern characterised by cardiometabolic risk factors, dysregulated adipokine signalling and inflammation. The study aimed to assess the serum levels of omentin and visfatin in patients with metabolic syndrome. METHODS: The 84-subject hospital-based case-control study included 18-55 years, both genders. Anthropometry, medical history, fasting plasma glucose (FPG), lipid profile, and HOMA-IR were collected. Insulin, omentin, and visfatin were measured using ELISA. RESULTS: Omentin and visfatin levels significantly differed between groups ( < 0.05). The median omentin levels were 50.74 and 45.25; visfatin levels were 0.064 and 0.001, respectively. Omentin correlated with waist circumference, blood pressure, and FPG in controls, while visfatin correlated with HDL and BMI among cases ( < 0.05). Omentin and visfatin were elevated in cases. However, no significant correlation between omentin and visfatin with lipid parameters could be established. CONCLUSION: Omentin and visfatin levels varied significantly between metabolic syndrome and controls; their correlation with MetS criteria was not significant.
PURPOSE: Bariatric surgery can effectively alleviate obesity and diabetes by regulation of the gut microbiota. This study aimed to investigate the change in the gut microbiota metabolite TMAO and to explore its effect on...PURPOSE: Bariatric surgery can effectively alleviate obesity and diabetes by regulation of the gut microbiota. This study aimed to investigate the change in the gut microbiota metabolite TMAO and to explore its effect on glucose metabolism after sleeve gastrectomy (SG). MATERIALS AND METHODS: Diet-induced obesity mouse models were established, and the mice were randomly divided into four groups: an SG group, a sham-operated group pair-fed with the SG group (PF), a sham-operated group fed ad libitum (AL), and a lean control group (C). At 10 weeks post-surgery, the changes in glycogen content of liver, gut microbiota and the level of FMO3 in the liver were evaluated, and their correlation with TMAO production was analysed. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. RESULTS: At 10 weeks post-surgery, hepatocyte glycogen levels were restored, and serum TMA and TMAO levels were significantly increased. Faecal metagenomic sequencing results showed that the abundances of Ruminococcaceae and Lachnospiraceae, which were positively correlated with TMAO production, were significantly increased after surgery. While the changes in FMO3, the key enzyme producing TMAO in the liver was found decreased significantly after SG. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. Inconsistent with the changing trend of TMAO, the expression of PERK, FOXO1, PCK, and G6PC significantly decreased after SG. CONCLUSIONS: SG can significantly reduce obesity and restore glucose metabolism. After surgery, TMAO metabolites increased in a microbiota-dependent manner.
BACKGROUND: The present study conducted to assess whether vitamin D (Vit D) could ameliorate the anxiety and depression induced by nicotine (Nic) withdrawal in male adult rats. METHODS: To this end, behavioural tests wer...BACKGROUND: The present study conducted to assess whether vitamin D (Vit D) could ameliorate the anxiety and depression induced by nicotine (Nic) withdrawal in male adult rats. METHODS: To this end, behavioural tests were done in male Wistar rats undergone adolescent Nic exposure (2 mg/kg) and then withdrawal and the effect of Vit D (100, 1000, and 10,000 IU/kg) was assessed at both behavioural and biochemical levels. RESULTS: Results indicated that Vit D treatment could effectively prevent anxiety, depression, and biochemical alterations induced by Nic withdrawal. CONCLUSION: Vit D has strong potential to be used for prevention of anxiety- and depressive-like behaviours following Nic withdrawal; however, further investigation is needed in larger sample size to discuss more confidently.
Bora J, Malik S, Mishra R
… +11 more, Rustagi S, Slama P, Lata S, Talukdar N, Alghamdi S, Aldairi A, Habiballah FN, Almehmadi M, Abdulaziz O, Alsiwiehri N, Ramniwas S
OBJECTIVE: This study investigates the in-vitro and in-vivo antioxidant capacities showed by Nees. () in alloxan-administered diabetic mice. MATERIALS AND METHODS: The screening of phytochemical of methanolic flower ext...OBJECTIVE: This study investigates the in-vitro and in-vivo antioxidant capacities showed by Nees. () in alloxan-administered diabetic mice. MATERIALS AND METHODS: The screening of phytochemical of methanolic flower extract (MFE), Gas Chromatography Mass Spectrometry (GC-MS) profiling was utilized to identify bioactive compounds. In-vitro antioxidant studies were performed. Acute toxicity was evaluated in mice. Glucose Transporter type 4 (GLUT4) protein expression and antioxidant enzyme activities were assessed. Histopathological examination of heart tissue was performed. RESULTS: GC-MS analysis revealed the presence of various bioactive compounds consisting of antioxidant, anti-inflammatory activities. The results also showed a noteworthy increase in in-vitro and in-vivo antioxidant enzymes activities. Moreover, MFE suppress hyperglycaemia by upregulating GLUT4 protein expression. In histological study MFE was found to restore cellular alterations in diabetic tissue. DISCUSSION AND CONCLUSION: It is inferred from the study that MFE of can exert a protective effect by suppressing hyperglycaemia and modulating oxidative stress in alloxan-administered diabetic mice.
ABSTARCTTo investigate the role and mechanism of miR-93 in apoptosis, migration, invasion and chemoresistance of diffuse large B-cell lymphoma (DLBCL) cells, bioinformatics and real-time quantitative reverse transcriptio...ABSTARCTTo investigate the role and mechanism of miR-93 in apoptosis, migration, invasion and chemoresistance of diffuse large B-cell lymphoma (DLBCL) cells, bioinformatics and real-time quantitative reverse transcription PCR were employed to detect the expression of miR-93 and SMAD5 in DLBCL tissues and cells. There was a notable upregulation of miR-93 expression in DLBCL samples. In DLBCL cells (OCI-LY7 and SU-DHL-8), miR-93 enhanced the chemoresistance to vincristine and inhibited apoptosis by increasing the expression of the anti-apoptotic protein Bcl-2 and decreasing cleaved caspase-3 levels. Additionally, miR-93 significantly reduced apoptosis rates and promoted cell migration and invasion. Collectively, miR-93 promoted malignant behaviour and increased chemoresistance of DLBCL cells by targeting and inhibiting SMAD5 expression. Thus, inhibiting miR-93 expression or elevating SMAD5 expression is likely to be crucial for DLBCL treatment.
BACKGROUND: Osteoporosis poses a global health challenge, particularly with an ageing population. Quercetin, isorhamnetin, avicularin, isoquercetin, quercitrin, and taxifolin are natural flavonoids with similar structure...BACKGROUND: Osteoporosis poses a global health challenge, particularly with an ageing population. Quercetin, isorhamnetin, avicularin, isoquercetin, quercitrin, and taxifolin are natural flavonoids with similar structure that induce ontogenesis. METHODS: In the present study, proteins in oestrogen signalling and bone morphogenesis were analysed, and hub genes were identified with Cytoscape, followed by pathway analysis. Then, molecular targets of flavonoids and osteoporosis-related targets were identified, and overlaps were detected. Molecular docking and dynamics simulations assessed flavonoid interactions with ERs. RESULTS: The study identified 14 gene products linked to osteoporosis, including ESR1 and ESR2. Enrichment analyses confirmed ESR involvement in various biological processes. SwissTargetPrediction highlighted quercetin and isorhamnetin as favourable targets for ESR1 and ESR2. Molecular docking and dynamics revealed favourable and stable binding of flavonoids to ERα and ERβ. CONCLUSIO: These interactions suggest therapeutic potential of natural flavonoids for osteoporosis treatment by targeting ERs, laying a foundation for future research in preclinical and clinical settings.
This study assessed the cardioprotective effects of <1 kDa peptide fractions from neem seed protein hydrolysates (NSPHs) in cardiac tissues . Oxidative injury was induced in cardiac tissues from male Wister rats by incub...This study assessed the cardioprotective effects of <1 kDa peptide fractions from neem seed protein hydrolysates (NSPHs) in cardiac tissues . Oxidative injury was induced in cardiac tissues from male Wister rats by incubating with 0.1 mM FeSO (pro-oxidant) for 30 minutes. Untreated tissues lacked peptide fractions, while normal control tissues lacked peptide and pro-oxidant. Treatment with the peptides increased the activities/levels of catalase, superoxide dismutase, ENTPDase, 5'NTPDase, glutathione, and HDL-cholesterol. Conversely, the levels/activities of malondialdehyde, nitric oxide, cholesterol, LDL-cholesterol, ACE, acetylcholinesterase, ATPase decreased following treatment with NSPH peptide fractions. Furthermore, the peptides depleted oxidative metabolites, while concomitantly inactivating plasmalogen synthesis and beta-oxidation of long-chain saturated fatty acids. These findings suggest that <1 kDa peptide fractions from neem seed protein hydrolysates have cardioprotective properties, potentially offering a natural therapeutic option for managing oxidative cardiac dysfunction through the regulation of oxidative stress, cholinesterase and purinergic activities, and lipid metabolism.
This study investigated the anti-atherogenic effects of leaves aqueous, hydro-ethanolic extracts, and ethyl acetate fraction at doses of 100, 200, and 400 mg/kg for 21 d. As results, at the dose of 400 mg/kg, the ethyl...This study investigated the anti-atherogenic effects of leaves aqueous, hydro-ethanolic extracts, and ethyl acetate fraction at doses of 100, 200, and 400 mg/kg for 21 d. As results, at the dose of 400 mg/kg, the ethyl acetate fraction significantly ( < .001) decreased the level of total cholesterol (112.52 ± 1.21 mg/dL), triglyceride (76.47 ± 0.97 mg/dL), and LDL-C (22.01 ± 2.92 mg/dL). Whereas, a significant ( < .001) increase was observed in the level of HDL-C (74.97 ± 1.99 mg/dL). Moreover, the atherogenic index significantly ( < .001) decreased (0.008 ± 0.00 mg/dL), while the percentage of atherogenic protection increased (99.13 ± 0.78%). The activity of antioxidant enzymes increased significantly ( < .001), while malondialdehyde concentration decreased. The thickening of aorta media (67.27 ± 7.15 µm) was also attenuated significantly ( < .001). Thus, our finding supports the use of for future atherosclerosis drug discovery.
OBJECTIVE: This study was to investigated the inhibitory role of the tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties and its underlying mechanisms. M...OBJECTIVE: This study was to investigated the inhibitory role of the tumour protein p53 (TP53)-activated PGM5-AS1 in lung cancer (LC) cell proliferation, invasion, and CSC-like properties and its underlying mechanisms. METHODS: The effect of PGM5-AS1 on LC cell development was determined. Stem cell markers, aldehyde dehydrogenase activity in cells were tested, as well as the ability of stem cells to form spheroids. The interaction of PGM5-AS1 and TP53 was determined. The binding link of PGM5-AS1, miR-1247-5p, and R-spondin1 (RSPO1) was verified. RESULTS: PGM5-AS1 was elevated by a combination of TP53 and PGM5-AS1 promoters. PGM5-AS1 was a molecular sponge of miR-1247-5p in LC cells, and miR-1247-5p targeted RSPO1. Elevating PGM5-AS1 or repressing miR-1247-5p restrained LC cell growth and stemness, which were reversed by depression of RSPO1. CONCLUSION: This study conveys that TP53-elevated PGM5-AS1 mediates miR-1247-5p to target RSPO1, thereby inhibiting LC growth and stemness, representing a novel avenue for LC therapy.
OBJECTIVE: This study explores the mechanism of methyltransferase like 3 (METTL3) on sepsis-associated encephalopathy (SAE)-induced hippocampal neuronal injury. METHODS: A murine model of SAE was established by caecal li...OBJECTIVE: This study explores the mechanism of methyltransferase like 3 (METTL3) on sepsis-associated encephalopathy (SAE)-induced hippocampal neuronal injury. METHODS: A murine model of SAE was established by caecal ligation and puncture. Hippocampal cells were induced by lipopolysaccharide (LPS). The mouse survival was observed and behavioural tests evaluated cognitive function. METTL3 and glutamic-oxaloacetic transaminase 1 (GOT1) expressions were detected via RT-qPCR and Western blot. Immunofluorescence staining examined the co-localization of NeuN and METTL3. The m6A enrichment on GOT1 was determined by MeRIP. RESULTS: METTL3 and GOT1 were highly expressed in SAE mice and LPS-stimulated hippocampal cells. SAE mice exhibited cognitive function impairment, reduced survival rate, and decreased neuronal cells. LPS induction increased hippocampal cell apoptosis and enhanced inflammation. Silence of METTL3 reduced hippocampal neuronal injury in SAE mice and LPS-induced hippocampal cell injury. CONCLUSION: METTL3-mediated m6A modification on GOT1 mRNA elevates GOT1 expression, thereby aggravating SAE-induced hippocampal neuronal injury.
OBJECTIVE: This study investigated bee bread's (BB) protective and therapeutic effects on acetic acid-(AA)-induced gastric ulcers via oxidative stress, DNA damage, inflammation, and apoptosis. MATERIALS AND METHODS: Rats...OBJECTIVE: This study investigated bee bread's (BB) protective and therapeutic effects on acetic acid-(AA)-induced gastric ulcers via oxidative stress, DNA damage, inflammation, and apoptosis. MATERIALS AND METHODS: Rats were administered saline-(1ml) or BB-(0.5g/kg/day;1ml) by oral gavage once daily for 10-day following 80% AA-induced chronic ulceration in treatment group. Pretreatment group received saline or BB for 10-day before and 3-day after ulcer induction. Stomachs of decapitated rats were collected for ulcer index, histological and biochemical analyses. RESULTS: BB significantly reduced the gastric ulcer index and levels of chemiluminescence, HMGB-1, IL-6, IL-1ß and IL-8 levels in pretreatment and treatment groups. In BB-pretreated ulcer group, MPO-(saline\BB, 39.9±3.7 U/g;22.2±2.2 U/g), caspase-3 (0.40±0.07 ng/g;0.18±0.01 ng/g) and IFN-γ (15.46±1.76;9.51±1.95 ng/g) levels decreased and TNF-α (31.77±5.13;18.94±2.59 ng/g) reduced only in BB-treated ulcer group. MDA, GSH, NRF-2, and 8-OHdG levels remained unchanged. CONCLUSION: BB has demonstrated protective and therapeutic effects by reducing ROS production, modulating inflammation and apoptosis.
INTRODUCTION: This study aimed to assess the expression changes of BTG1, PGI, and PGII in tissues and serum of patients with gastric cancer, atrophic gastritis, and healthy individuals. METHODS: QRT-PCR was used to measu...INTRODUCTION: This study aimed to assess the expression changes of BTG1, PGI, and PGII in tissues and serum of patients with gastric cancer, atrophic gastritis, and healthy individuals. METHODS: QRT-PCR was used to measure BTG1, PGI, and PGII expression in 30 cancers, 30 atrophic gastritis, and 30 healthy tissue samples. Serum levels of PGI and PGII were measured using ELISA. Statistical tests included the Mann-Whitney U and independent T-test. Covariates like tumour stage and status were considered. RESULTS: BTG1 expression was significantly lower in cancer and gastritis tissues. Serum PGI and PGII levels were significantly reduced in cancer patients ( ≤ 0.001). DISCUSSION: The PGI/PGII ratio in serum emerged as a strong non-invasive biomarker for distinguishing cancer from healthy individuals. While BTG1 provides insights into gastric carcinogenesis, its clinical utility is limited due to the need for tissue samples. The serum-based PGI/PGII ratio shows greater promise as a non-invasive screening tool for GC.
Diabetic retinopathy (DR) is the leading manifestation of diabetic microangiopathy. However, effective biomarkers and therapies are lacking. Circular RNAs (circRNAs) have been implicated in various diseases including DR....Diabetic retinopathy (DR) is the leading manifestation of diabetic microangiopathy. However, effective biomarkers and therapies are lacking. Circular RNAs (circRNAs) have been implicated in various diseases including DR. However, the role of circRNAs in DR remains elusive. In the present study, circNXN was upregulated in high glucose (HG)-treated human retinal microvascular endothelial cells (hRMECs). circNXN knockdown inhibited the proliferation, migration, and angiogenesis of hRMECs and promoted apoptosis. In addition, circNXN acted as a sponge for miR-338-3p to facilitate the FGFR1 (fibroblast growth factor receptor 1) expression. Furthermore, rescue assays revealed that the reduced promoting effect on hRMECs induced by the knockdown of circNXN could be reversed by a miR-338-3p inhibitor in HG-treated hRMECs. Additionally, in a DR rat model, circNXN downregulation ameliorated retinal vasculature changes. Our findings reveal a new therapeutic strategy for DR that may provide a new approach to clinical DR therapy.