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Antioxidant Mediated Defense Role of the Dietary Phytochemical Ferulic Acid, against Carbon Tetrachloride (CCl4) Induced Toxic Hepatitis

机译:膳食植物化学阿魏酸对四氯化碳(CCl4)诱导的中毒性肝炎的抗氧化介导防御作用

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Ferulic acid (FA) is a dietary phytochemical formed during the metabolism of phenylalanine and tyrosine. Disruption of mitochondria and free radical mediated tissue injury has been reported during liver toxicity induced by carbon tetrachloride, potent hepatotoxic agent. The present study was designed to investigate the antioxidant protective effect of ferulic acid on hepatocytes, liver function and mitochondrial electron respiratory chain enzymes in hepatotoxic rats. Rats were classified into four groups : normal control group, hepatotoxic group subcutaneously injected with CCl4 once weekly for 4 weeks; third group: hepatotoxic group daily administered orally FA with a dose of 20 mg/Kg b.wt., and forth group: hepatotoxic group daily administered orally FA with a dose of 80 mg/Kg b.wt. The model of CCl4-injected hepatocellular rats elicited declines in liver antioxidant enzyme activities; glutathione peroxidase, superoxide dismutase , Catalase in association of a reduction in reduced glutathione, serum total protein with concomitant significant elevations in lipid peroxidation marker , serum nitric oxide,and liver enzymes, lactate dehydrogenase and total bilirubin. CCl4 resulted in a significant decrease in the activities of mitochondrial respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase). FA enhanced the attenuation of these functional abnormalities and restored normal mitochondrial function when compared to rats CCl4 toxicant treated groups , the attenuating effect was more pronounced in FA low dose Hence, these findings demonstrate the ameliorative role of FA on mitochondrial function during CCl4 induced hepatotoxicity and associated oxidative stress in rats.
机译:阿魏酸(FA)是在苯丙氨酸和酪氨酸代谢过程中形成的饮食植物化学物质。据报道,在四氯化碳(一种有效的肝毒剂)引起的肝毒性过程中,线粒体破坏和自由基介导的组织损伤。本研究旨在研究阿魏酸对肝毒性大鼠肝细胞,肝功能和线粒体电子呼吸链酶的抗氧化保护作用。大鼠分为四组:正常对照组,肝毒性组,每周皮下注射CCl4,持续4周。第三组:肝毒性组,每天口服FA的剂量为20 mg / Kg b.wt.,第四组:肝毒性组,每天口服FA的剂量为80 mg / Kgb.wt。注射CCl 4 的肝细胞大鼠模型引起肝脏抗氧化酶活性下降。谷胱甘肽过氧化物酶,超氧化物歧化酶,过氧化氢酶与减少的谷胱甘肽减少,血清总蛋白伴有脂质过氧化标记物,血清一氧化氮和肝酶显着升高有关,乳酸脱氢酶和总胆红素。 CCl 4 导致线粒体呼吸链酶(NADH脱氢酶和细胞色素C氧化酶)的活性显着降低。与大鼠CCl 4 毒物治疗组相比,FA增强了这些功能异常的衰减并恢复了正常的线粒体功能,在低剂量的FA中衰减作用更为明显,因此,这些发现证明了FA的改善作用对CCl 4 诱导的大鼠肝毒性及相关氧化应激过程中线粒体功能的影响

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