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Gallic acid protects against Aflatoxin B1 -induced oxidative and inflammatory stress damage in rats kidneys and liver.
Journal of Food Biochemistry ( IF 3.5 ) Pub Date : 2020-06-04 , DOI: 10.1111/jfbc.13316 Solomon Owumi 1 , Eseroghene S Najophe 2 , Ebenezer O Farombi 3 , Adegboyega K Oyelere 4
Journal of Food Biochemistry ( IF 3.5 ) Pub Date : 2020-06-04 , DOI: 10.1111/jfbc.13316 Solomon Owumi 1 , Eseroghene S Najophe 2 , Ebenezer O Farombi 3 , Adegboyega K Oyelere 4
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The adverse effect of Aflatoxin B1 (AFB1) exposure in both humans and rodents has been widely reported. The beneficial health effects of gallic acid (GA) against AFB1‐induced toxicity in vitro have been published. Here, we present in vivo findings on AFB1 and GA on hepatorenal function in rats, exposed to AFB1 (75 µg/kg body weight) only or co‐treated with GA (20 or 40 mg/kg) for 28 successive days. AFB1 significantly increased pro‐inflammatory biomarkers and suppressed IL‐10 levels in rats’ liver and kidney. AFB1 caused increased (p < .05) oxidative stress by decreasing antioxidant enzymes levels and increasing levels of reactive oxygen and nitrogen species. Furthermore, reduction (p < .05) in cellular glutathione (GSH) levels and increased (p < .05) hepatorenal markers of toxicity were detected in rats treated with AFB1. These observed alterations were, however, reversed in GA co‐treated rats. GA ameliorated AFB1‐induced hepatorenal dysfunction by decreasing oxidative stress and inflammation in rats.
中文翻译：
没食子酸可防止黄曲霉毒素B1诱导的大鼠肾脏和肝脏的氧化和炎症应激损伤。
黄曲霉毒素B1（AFB 1）暴露对人类和啮齿类动物的不利影响已得到广泛报道。没食子酸（GA）对AFB 1诱导的体外毒性的有益健康作用已经发表。在这里，我们介绍了AFB 1和GA对大鼠肝肾功能的体内发现，仅暴露于AFB 1（75 µg / kg体重）或与GA（20或40 mg / kg）连续治疗28天。AFB 1显着增加了大鼠肝脏和肾脏的促炎生物标志物并抑制了IL-10水平。AFB 1引起的增加（p <.05）通过降低抗氧化酶水平和增加活性氧和氮物种的水平来产生氧化应激。此外， 在用AFB 1处理的大鼠中，检测到 细胞谷胱甘肽（GSH）水平降低（p <.05）和肝肾毒性标记物升高（p <.05）。然而，在GA联合治疗的大鼠中，这些观察到的改变被逆转了。GA通过降低大鼠的氧化应激和炎症改善了AFB 1诱导的肝肾功能不全。
更新日期：2020-06-04
中文翻译：
没食子酸可防止黄曲霉毒素B1诱导的大鼠肾脏和肝脏的氧化和炎症应激损伤。
黄曲霉毒素B1（AFB 1）暴露对人类和啮齿类动物的不利影响已得到广泛报道。没食子酸（GA）对AFB 1诱导的体外毒性的有益健康作用已经发表。在这里，我们介绍了AFB 1和GA对大鼠肝肾功能的体内发现，仅暴露于AFB 1（75 µg / kg体重）或与GA（20或40 mg / kg）连续治疗28天。AFB 1显着增加了大鼠肝脏和肾脏的促炎生物标志物并抑制了IL-10水平。AFB 1引起的增加（p <.05）通过降低抗氧化酶水平和增加活性氧和氮物种的水平来产生氧化应激。此外， 在用AFB 1处理的大鼠中，检测到 细胞谷胱甘肽（GSH）水平降低（p <.05）和肝肾毒性标记物升高（p <.05）。然而，在GA联合治疗的大鼠中，这些观察到的改变被逆转了。GA通过降低大鼠的氧化应激和炎症改善了AFB 1诱导的肝肾功能不全。
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