Search

The present study explored the ameliorative potency of aqueous extract of Capsicum annum (AqCA), against oxidative imbalance and renal toxicity induced by ethanol. Randomly grouped male Wistar rats (n = 6), were marked as ethanol‐treated (2 g/kg bw, i.p.), CA125 (125 mg/kg bw, i.p.), CA250 (250 mg/kg bw, i.p.), ethanol pre‐treated with CA (similar doses), and control (0.5 ml normal saline, i.p.), and treated for 30 consecutive days. Biochemical analysis of tissue and serum parameters was performed, along with histopathological and histochemical studies. Also, we performed TUNEL assay and western blotting for our experimental groups. Statistical analysis revealed significant (p ≤.001) alteration in the levels of antioxidant enzymes, serum urea, creatinine, pro‐inflammatory cytokines, and cleaved caspases, along with histopathological alterations in the ethanol‐treated group. Prior treatment with AqCA prevented ethanol‐induced alterations in tissue and serum parameters. These findings indicate that the extract of CA can protect renal cells from ethanol‐induced damage by inhibiting oxidative stress, inflammatory response, and apoptosis. Practical applications: Chronic alcohol consumption is a major public health concern that leads to various diseases and social problems as well. It affects both the affluent and non‐affluent society equally. Alcohol (ethanol) is a renowned hepato‐toxicant and a well‐documented risk factor for oxidative stress, with less known effect on the kidney. Thus, it is essential to investigate the effect of alcohol metabolism on the kidney to find a remedy to prevent it. The present investigation depicts the anti‐oxidative and anti‐inflammatory role of Capsicum annum against ethanol‐induced renal damage. The outcome of this study can be utilized in the future for phytotherapeutic herbal drug formulation. Besides, the bioactive components identified in the study can be further explored by researchers or pharmaceutical corporates for potential therapeutic purpose against renal impairment. [ABSTRACT FROM AUTHOR]

Accumulation of neurotoxic bilirubin due to a transient neonatal or persistent inherited deficiency of bilirubin glucuronidation activity can cause irreversible brain damage and death. Strategies to inhibit bilirubin production and prevent neurotoxicity in neonatal and adult settings seem promising. We evaluated the impact of Bvra deficiency in neonatal and aged mice, in a background of unconjugated hyperbilirubinemia, by abolishing bilirubin production. We also investigated the disposal of biliverdin during fetal development. In Ugt1−/− mice, Bvra deficiency appeared sufficient to prevent lethality and to normalize bilirubin level in adults. Although biliverdin accumulated in Bvra-deficient fetuses, both Bvra−/− and Bvra−/−Ugt1−/− pups were healthy and reached adulthood having normal liver, brain, and spleen histology, albeit with increased iron levels in the latter. During aging, both Bvra−/− and Bvra−/−Ugt1−/− mice presented normal levels of relevant hematological and metabolic parameters. Interestingly, the oxidative status in erythrocytes from 9-months-old Bvra−/− and Bvra−/−Ugt1−/− mice was significantly reduced. In addition, triglycerides levels in these 9-months-old Bvra−/− mice were significantly higher than WT controls, while Bvra−/−Ugt1−/− tested normal. The normal parameters observed in Bvra−/−Ugt1−/− mice fed chow diet indicate that Bvra inhibition to treat unconjugated hyperbilirubinemia seems safe and effective. [ABSTRACT FROM AUTHOR]