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Curcumin protects sodium nitrite-induced hepatotoxicity in Wistar rats

机译:姜黄素可保护亚硝酸钠诱导的Wistar大鼠肝毒性

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摘要

In this study, the protective effect of curcumin on sodium nitrite (NaNO2) induced hepatotoxicity was assessed in male Wistar rats. Wistar rats were administered orally daily with 20 mg/kg of curcumin for 28 days and NaNO2 was administered as a single dose of 60 mg/kg on day 28. Lipid profile, liver function biomarkers and C-reactive protein were assessed in the serum; lipid peroxidation, non-enzymatic and enzymatic antioxidants were assessed in the liver. Alanine amino transferases (94.67 U/L), aspartate amino transferases (194.33 U/L), alkaline phosphatases, C-reactive proteins (19.56 ng/L) and lipid peroxidation (8.03 × 10−6 μmol/mg protein) were significantly elevated (P < 0.05), while a significant decrease in lipid profiles (total cholesterol, HDL,LDL, and triglycerides): (0.61,0.37, 0.4 and 0.47 mg/dl respectively), reduced glutathione level (4.16 μmol/mg protein), and decreased catalase, superoxide dismutase and glutathione peroxidase activities with severe histological alterations were observed in the livers of rats exposed to NaNO2. Pre-treatment with curcumin significantly (P < 0.05) prevented these alterations by adjusting the lipid profile, liver function markers, and C-reactive proteins and abrogating the elevated markers of oxidative stress as supported by the liver histology. This suggests that dietary consumption of curcumin is beneficial against NaNO2 induced oxidative stress of the liver via its antioxidant potential.
机译:在这项研究中,在雄性Wistar大鼠中评估了姜黄素对亚硝酸钠(NaNO2)诱导的肝毒性的保护作用。 Wistar大鼠每天口服20μg/ kg姜黄素,持续28天,NaNO2在第28天以60μmg/ kg的单次剂量给予。评估血清中的脂质谱,肝功能生物标志物和C反应蛋白。在肝脏中评估脂质过氧化,非酶抗氧化剂和酶抗氧化剂。丙氨酸氨基转移酶(94.67 U / L),天冬氨酸氨基转移酶(194.33 U / L),碱性磷酸酶,C反应蛋白(19.56 ng / L)和脂质过氧化(8.03×10 −6 μmol / mg蛋白)显着升高(P <0.05),而脂质谱(总胆固醇,HDL,LDL和甘油三酸酯)显着降低:(分别为0.61,0.37、0.4和0.47 mg / dl),降低了谷胱甘肽水平(在暴露于NaNO2的大鼠肝脏中,观察到4.16μmol/ mg蛋白),过氧化氢酶,超氧化物歧化酶和谷胱甘肽过氧化物酶活性降低,并伴有严重的组织学改变。姜黄素预处理(P <0.05)可通过调节脂质分布,肝功能标志物和C反应蛋白并消除肝脏组织学支持的氧化应激升高标志物来防止这些改变。这表明饮食中食用姜黄素可通过其抗氧化潜力对抗NaNO2诱导的肝脏氧化应激。

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