Archives of Physiology and Biochemistry最新文献

Objective: This study aimed to investigate the effects of circ-RPL15 on epithelial mesenchymal transformation (EMT) and tumour growth in non-small cell lung cancer (NSCLC).

Methods: circ-RPL15, microRNA (miR)-518c-3p and WD repeat protein 1 (WDR1) in tumour tissues were detected. Cell viability, apoptosis, migration and invasion, and EMT were analysed in A549 cells after altering circ-RPL15 or miR-518c-3p expression. The targeting relationship between miR-518c-3p with circ-RPL15 or WDR1 was verified.

Results: The results elucidated that circ-RPL15 and WDR1 levels were elevated in NSCLC tissues, while miR-518c-3p was downregulated. Suppressing circ-RPL15 or elevating miR-518c-3p suppressed cell growth and delayed EMT process. miR-518c-3p was found to target both circ-RPL15 and WDR1, and increasing WDR1 counteracted the effects of reducing circ-RPL15 on A549 cells. Downregulating circ-RPL15 suppressed tumour growth in NSCLC in vivo.

Conclusion: Shortly, circ-RPL15 accelerates EMT and tumour growth in NSCLC via modulating the miR-518c-3p/WDR1 axis.

Chronic sinusitis with nasal polyps (CRSwNP) has a relatively high recurrence rate, seriously affecting the quality of life of patients. Neuroinflammation interacts with the persistent inflammatory state of the nasal mucosa. This study aims to explore the application value of medical thermal imaging technology in predicting postoperative recurrence of nECRSwNP, and to evaluate potential biomarkers and efficacy assessment methods for neuroinflammation treatment, with the expectation of providing new strategies for reducing postoperative recurrence rates and improving the quality of life. Medical thermal imaging technology can monitor the temperature changes of nasal mucosa in real time and promptly detect alterations in inflammatory activity. The levels of EOS and cytokines in peripheral blood can serve as potential biomarkers for evaluating the status of neuroinflammation, which is helpful for identifying patients with a higher risk of recurrence, thereby enabling timely adjustment of treatment plans and improving the pertinence and effectiveness of neuroinflammation treatment.

Kidney injury is a common complication of obesity. This study evaluated the protective effect of the prebiotic fructooligosaccharide (FOS) on kidney injury in a high-fat diet-induced obese rat model. Obese rats exhibited increased body weights, elevated lipid profiles, decreased plasma lipopolysaccharide-binding protein (LBP), elevated kidney malondialdehyde (MDA), increased superoxide dismutase (SOD) activity, and histopathological damage. They also show reduced nephrin expression and upregulated mRNA levels of kidney injury molecule-1 (KIM-1) and renin. Supplementation with 10% FOS significantly reduced body weight and triglyceride levels, restored plasma LBP, decreased kidney MDA levels, and enhanced SOD activity. FOS also prevented the upregulation of KIM-1 and renin mRNA and restored nephrin expression. These findings suggest that FOS mitigates obesity-induced kidney injury, supporting its potential as a preventive nutritional intervention.

Background: Metabolic syndrome (MetS) involves insulin resistance and dyslipidemia.

Objective: To evaluate vitamin D's (Vit D) hepatoprotective role in MetS and its mechanisms.

Methods: Thirty male rats were divided into MetS, MetS + Vit D, and control groups. We measured arterial blood pressure (ABP), body weight, fat, homeostatic Model Assessment for Insulin Resistance (HOMA-IR), glycemic/lipid profiles, liver enzymes, oxidative stress (Malondialdehyde, superoxide dismutase), inflammation (Tumor necrosis factor; TNF-α, matrix metalloproteinase; MMP9, Glial fibrillary acidic protein; GFAP), and AMP-activated protein kinase/Phosphoinositide 3-kinase (AMPK/PI3K) expression.

Results: MetS increased oxidative stress, TNF-α, liver enzymes, HOMA-IR, and ABP while reducing adiponectin and AMPK/PI3K. Vit D reversed these effects, suppressing GFAP/MMP9 and restoring metabolic balance. Conclusion: Vit D mitigates MetS-induced liver damage via AMPK/PI3K activation, exerting antioxidant and anti-inflammatory effects.

Context: Diabetic cardiomyopathy (DCM) is a chronic cardiac disorder that develops independently of coronary artery disease or hypertension in individuals with diabetes. Despite being identified over fifty years ago, it remains poorly recognized, and its management lacks standardization. The rising global prevalence of diabetes has amplified the incidence of DCM, underscoring the urgent need to clarify its molecular underpinnings and clinical progression.

Objective: To provide a comprehensive review of the molecular and physiological mechanisms underlying diabetic cardiomyopathy, elucidating how metabolic dysregulation contributes to cardiac structural and functional alterations. This study also aims to highlight the potential therapeutic targets involved in the key signaling pathways of DCM pathogenesis.

Methods: A systematic literature review was conducted using major scientific databases, including PubMed, Scopus, and Web of Science, covering studies published between 2000 and 2025. Keywords used included "diabetic cardiomyopathy," "hyperglycemia," "insulin resistance," "oxidative stress," "inflammation," "mitochondrial dysfunction," and "therapeutic targets."

Data sources, study selection, and data extraction: Peer-reviewed articles, original research papers, and review articles focusing on molecular mechanisms, signaling pathways, and therapeutic interventions related to DCM were included. Studies involving both experimental models and human subjects were considered. Data were extracted regarding metabolic alterations, key signaling cascades (NF-κB, PARP1, GLUT4, AT1R), and their association with cardiac remodeling, fibrosis, and functional impairment. The information was synthesized to illustrate the progression from metabolic imbalance to clinical manifestations and to identify promising molecular targets for therapy.

Objective: Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme with many essential biochemical functions. However, in various cancer diseases, increased activity of G6PD causes cancer cells to grow, so G6PD inhibitors have become a significant area of research in cancer treatment.

Materials and methods: Here, G6PD was purified 4530-fold with affinity chromatography using 2',5'-ADP Sepharose 4B from sheep liver. The effects of reduced glutathione (GSH) and ascorbic acid (vitamin C) on G6PD activity were explored.

Results and discussion: GSH and ascorbic acid showed a significant inhibitory effect on G6PD, and IC₅₀ values were found as 0.37 µM and 34.66 µM, respectively. The inhibition type from Lineweaver-Burk plots of these compounds was identified as non-competitive inhibition. The K_i values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively.

Conclusion: In this study, it was observed that GSH and ascorbic acid antioxidant compounds exhibit an inhibitory effect on G6PD and may be protective and preventive against cancer.

Background: Any toxicity initially damages the hepatic system, followed by renal dysfunction. Previously, it was established that carbon tetrachloride (CCl₄) intoxication severely damaged hepatocytes. Moreover, CCl₄-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 CCl₄ 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 CCl₄ intoxicated group, while IL-10 and TGF-β were significantly decreased 84.65% and 66.36%, respectively. CCl₄ 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 (p<0.001, p<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: This study aimed to investigate the possible protective effect of cholecalciferol against testicular dysfunction in L-thyroxine-induced hyperthyroid rat model.

Methods: Twenty-four adult male rats were divided into three groups: control, hyperthyroid, and hyperthyroid cholecalciferol treated. At the end of four weeks, serum samples were collected for measurement of thyroid hormones, testosterone, and serum inflammatory markers (interleukin-6 and tumour necrosis factor-alpha). Thereafter, malondialdehyde and antioxidant enzymes were assessed in the testicular homogenate. Also, histological and immunohistochemical studies of the testicular tissues were done.

Results: The current results showed lower serum testosterone and testes weight in hyperthyroid rats than control group, with significantly elevated serum inflammatory markers, and disturbed oxidant/antioxidant status in the testicular tissues. This was associated with structural abnormalities. Immunohistochemical study showed upregulation of caspase-3 and downregulation of proliferating cell nuclear antigen (PCNA) in hyperthyroid rats. Cholecalciferol supplementation significantly improved the testicular dysfunction and the testicular pathological features in the hyperthyroid rats. It significantly decreased the levels of serum inflammatory markers and malondialdehyde levels. Also, cholecalciferol supplementation increased the activity of the antioxidant enzymes in the testicular tissue, downregulated caspase-3 and upregulated PCNA in the testicular tissues.

Conclusion: Cholecalciferol could ameliorate pathophysiological changes in rat testes of hyperthyroid rats.

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; p = 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; p = 0.025). The difference in serum PIVKA-II concentration was statistically significant between the controls, stage I-II patients, and stage III-IV patients (p < 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 p 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.

Aims: High-fat diet (HFD) consumption contributes to obesity and liver damage, while exercise training may counteract these effects. Given the regulatory role of microRNAs in lipid metabolism, this study investigates the impact of high-intensity interval training (HIIT) and HFD on hepatic fat accumulation, as well as the expression of miRNA-34a, miRNA-467b, and their associated proteins.

Main methods: Twenty-four male rats were randomly assigned to four groups: (1) CON, (2) HIIT, (3) HFD, and (4) HIIT+HFD. The HFD groups received a 60% fat diet, while the rats in the HIIT groups performed high-intensity interval training (3 sessions/week, 2.5 minutes high-intensity running × 90% maximal running capacity (MRC) with 2.5 minutes active rest × 50% MRC, for ten weeks). Forty-eight hours post-intervention, blood and liver samples were collected to assess histopathology, liver enzymes, and the expression of miRNA-34a, miRNA-467b, SIRT1, PPAR-ɑ, and LPL proteins.

Key findings: The HFD group exhibited excessive hepatic lipid accumulation, whereas HIIT significantly prevented HFD-induced hepatic steatosis, as confirmed by histopathological examinations. Liver enzyme levels (AST, ALT, and ALP) were significantly higher in the HFD group and significantly lower in both the HIIT and HIIT+HFD groups. Additionally, HIIT significantly increased miRNA-467b, SIRT1, and PPAR-ɑ expression while significantly decreasing miRNA-34a and LPL expression, preventing the effects of HFD.

Significance: Our findings identified a novel molecular mechanism confirming that HIIT is beneficial to prevent hepatic steatosis and hepatic damage induced by HFD, likely due to the modulation of miRNA-467b, miRNA-34a, and their main target proteins.