Chronic alcohol consumption exacerbates kidney injury, particularly in individuals with hepatitis B virus (HBV) infection. This study investigated the protective effects of boric acid supplementation against alcohol-induced renal damage in HBV transgenic mice. HBV transgenic mice were divided into four groups: control (C), boric acid (B), alcohol (A), and alcohol + boric acid (A + B). Renal injury was evaluated using H&E, PAS, TUNEL, and desmin staining. The expression of caspase-3, cytochrome c, and APAF-1 was analyzed by qRT-PCR. Biochemical analyses included BUN, creatinine, oxidative stress markers (ROS, MDA, TOS, OSI), total antioxidant status, and antioxidant enzyme activities (SOD, CAT, GPx). Histopathological findings showed activated parietal epithelial cells in all groups, indicating renal injury. Alcohol significantly increased tubular damage, podocyte desmin expression, apoptosis, cytochrome c and APAF-1 mRNA levels, and oxidative stress markers, while reducing antioxidant enzyme activities and BUN levels compared with controls. Boric acid supplementation significantly mitigated alcohol-induced tubular injury, apoptosis, oxidative stress, and serum creatinine levels, and improved BUN values. Boric acid treatment alone also alleviated glomerular and tubular injury and reduced tubular apoptosis compared with HBV control mice. Overall, boric acid exerts renoprotective effects in HBV-transgenic mice subjected to chronic alcohol exposure by inhibiting oxidative stress, apoptosis, and podocyte injury.

Background: Ischemia/reperfusion (I/R) injury is a clinical condition with high mortality, and an effective treatment strategy has yet to be established. Methods: This study was conducted on a total of 48 rats. They were divided into 6 groups of 8 rats each. Rats in Group S underwent laparotomy alone, while all other groups underwent laparotomy along with SMA I/R damage. Rats in Group B received 2 mg/kg/3 mL bupivacaine, rats in Group M received 0.5 mg/kg/3 mL morphine, rats in Group BM received 2 mg/kg/2 mL bupivacaine + 0.5 mg/kg/1 mL morphine, and rats in Group BML received 2 mg/kg/2 mL bupivacaine + 0.25 mg/kg/1 mL morphine subcutaneously. At the end of the study, blood samples were taken from all rats for oxidative stress parameters, ischemia markers, and cortisol measurement, and histopathological examination was performed. Results: Statistically significant differences were found among the groups with respect to mean total oxidant status (TOS), mean total antioxidant status (TAS), mean oxidative stress index (OSI), mean ischemia-modified albumin (IMA), and mean malondialdehyde (MDA) values ( p < 0.001). Statistically significant differences were also observed among the groups in terms of mean corticosterone and cortisol levels ( p < 0.001). Significant differences were found among the groups regarding mean intestinal histopathology score (IHS) and mean liver histopathology score (LHS) (respectively; p = 0.021, p = 0.002). Conclusions: The combination of morphine and bupivacaine provides effective analgesia and significantly improves oxidative stress parameters. The combined use of morphine and bupivacaine in infiltration anesthesia may be a promising treatment strategy for preventing I/R injury.

Multiple sclerosis is a chronic immune-mediated central nervous system disorder marked by neuroinflammation, demyelination, and neurodegeneration, and effectively modeled by experimental autoimmune encephalomyelitis. The objective of this study was to elucidate the roles of T follicular helper and T follicular regulatory cells in the progression of experimental autoimmune encephalomyelitis and to assess their association with IL-21 expression and central nervous system tissue pathology. In this study, experimental autoimmune encephalomyelitis was induced in 25 adult female C57BL/6 mice. Fluorescent double immunostaining for CXCR5 in combination with PD-1, ICOS, CD4, and FOXP3 was performed, along with the analysis of IL-21 mRNA expression. Histopathological assessment was conducted on the cerebrum, cerebellum, and medulla spinalis to evaluate neuroinflammation and myelin loss. A significant increase in CXCR5⁺PD-1⁺ and CXCR5⁺ICOS⁺ T follicular helper-like cells was observed in brain tissue, indicating immune activation and T follicular helper cell involvement. Simultaneously, a marked decrease in FOXP3⁺ T follicular regulatory-like cells suggested impaired immune tolerance and enhanced autoimmune activity. The infiltration of T follicular helper-like cells was identified as a key driver of inflammation and demyelination in the central nervous system. Additionally, the elevated IL-21 mRNA expression highlighted B cell activation and the initiation of antibody-mediated responses. These findings suggest that dysregulation of the T follicular helper/T follicular regulatory axis and elevated IL-21 expression contribute to the immunopathogenesis of experimental autoimmune encephalomyelitis, providing further insight into the mechanisms underlying multiple sclerosis development.