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首页> 外文期刊>Toxicology Reports >Curcumin protects sodium nitrite-induced hepatotoxicity in Wistar rats
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Curcumin protects sodium nitrite-induced hepatotoxicity in Wistar rats

机译:姜黄素在Wistar大鼠中保护亚硝酸盐诱导的肝毒性

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In this study, the protective effect of curcumin on sodium nitrite (NaNOsub2/sub) induced hepatotoxicity was assessed in male Wistar rats. Wistar rats were administered orally daily with 20?mg/kg of curcumin for 28 days and NaNOsub2/sub 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?×?10sup?6/sup?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 NaNOsub2/sub. 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 NaNOsub2/sub induced oxidative stress of the liver via its antioxidant potential.
机译:在该研究中,在雄性Wistar大鼠中评估了姜黄素对亚硝酸钠钠(纳米<亚> 2 )诱导的肝毒性的保护作用。每日口服施用Wistar大鼠28天,纳米 2 在第28天施用纳米 2 / kg。脂质曲线,肝功能生物标志物和肝功能在血清中评估C-反应蛋白;在肝脏中评估脂质过氧化,非酶促和酶促抗氧化剂。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(19.56Ω·Ng / L)和脂质过氧化(8.03?×10 ?6 μmol/ mg蛋白质)显着升高(p≤0.05),同时脂质曲线的显着降低(总胆固醇,HDL,LDL和甘油三酯):(0.61,0.37,0.4和0.47?mg / DL分别),在暴露于纳米 2 的大鼠肝脏中,观察到降低谷胱甘肽水平(4.16Ωμmol/ mg蛋白),降低过氧化氢酶,过氧化物酶,超氧化物歧化酶和谷胱甘肽过氧化物酶活性,大鼠肝脏肝脏。用姜黄素预处理(p≤0.05)通过调节脂质曲线,肝功能标记和C反应蛋白并消除肝脏组织学支持的氧化应激的升高标记来防止这些改变。这表明姜黄素的饮食消耗是有益于纳米<亚磷酸盐的抗氧化潜力肝脏的氧化胁迫。

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