article · Journal of Medicinal Food
Cyclosporine A (CsA) is a powerful immunosuppressant drug most widely used in managing organ transplantation and autoimmune diseases. The aim of this work was to investigate the role of taurine in alleviating the apoptotic hepatocytes and oxidative stress caused by CsA in rats' livers. The four experimental groups were evaluated, including (GpI) vehicle control (olive oil), (GpII) Tau (5 mg/kg/day), (GpIII) CsA (50 mg/kg/day), and (GpIV) CsA + Tau. The biochemical assay in liver functions and antioxidant enzymes was assayed, and the histopathology of hepatic tissue and immunohistochemical staining of apoptotic protein (p53) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) were determined. Induction of CsA in rats caused severe hepatotoxicity, as evidenced by the elevation of serum aspartate aminotransferase, alanine aminotransferase activities, and alkaline phosphatase concentration and decreased catalase (CAT), glutathione peroxidase, and glutathione reductase activities. The histopathological examination revealed mild to marked disorganization in the liver tissue, characterized by hepatocyte degeneration/necrosis, apoptotic hepatocytes, sinusoidal dilatation, and inflammatory cell infiltration. Whereas Tau treatment improved the liver function enzymes and increased the oxidative stress by elevating the antioxidant enzyme CAT and glutathione reductase. There is recovery of destructive liver tissue preserved hepatic trabecular architecture; dark nuclei with prominent nucleoli, hepatocytes, and mild dilated sinusoids; small area of pyknotic hepatocytes have vacuolated cytoplasm was seen, and the number of apoptotic cells detected by TUNEL and p53 protein was significantly decreased (<i>P</i> = .001). The results may contribute to the hepatoprotective role of Tau and its ability to ameliorate the oxidative stress and alleviate the apoptotic hepatocytes induced by CsA. So, Tau may have had a beneficial role in reducing tissue damage in patients exposed to CsA.
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DOI: 10.1177/1096620x251359940
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