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• W3159802010 abstract "Cholestasis is a serious complication affecting other organs such as the liver and kidney. Oxidative stress and mitochondrial impairment are proposed as the primary mechanisms for cholestasis-induced organ injury. Taurine (TAU) is the most abundant free amino acid in the human body, which is not incorporated in the structure of proteins. Several pharmacological effects have been attributed to TAU. It has been reported that TAU effectively mitigated oxidative stress and modulated mitochondrial function. The current study aimed to evaluate the impact of TAU on oxidative stress biomarkers and mitochondrial parameters in the kidney of cholestatic animals.Bile duct ligated (BDL) rats were used as an antioxidant model of cholestasis. Animals were treated with TAU (500 and 1000 mg/kg, oral) for seven consecutive days. Animals were anesthetized (thiopental 80 mg/kg, i.p.), and kidney and blood specimens were collected.Severe elevation in serum and urine biomarkers of renal injury was evident in the BDL group. Significant lipid peroxidation, reactive oxygen species (ROS) formation, and protein carbonylation were detected in the kidney of BDL animals. Furthermore, depleted glutathione reservoirs and a significant decrease in the antioxidant capacity of renal tissue were detected in cholestatic rats. Renal tubular atrophy and interstitial inflammation were evident in BDL animals. Cholestasis also caused significant mitochondrial dysfunction in the kidney. TAU significantly prevented cholestasis-induced renal injury by inhibiting oxidative stress and mitochondrial impairment.These data indicate TAU as a potential therapeutic agent in the management of cholestasis-induced renal injury." @default.
• W3159802010 created "2021-05-10" @default.
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• W3159802010 date "2021-01-01" @default.
• W3159802010 modified "2023-09-30" @default.
• W3159802010 title "Taurine mitigates bile duct obstruction-associated cholemic nephropathy: effect on oxidative stress and mitochondrial parameters" @default.
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• W3159802010 doi "https://doi.org/10.5114/ceh.2021.104675" @default.
• W3159802010 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8122090" @default.
• W3159802010 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34027113" @default.
• W3159802010 hasPublicationYear "2021" @default.
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