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Hepatoprotective role of berberine against paraquat-induced liver toxicity in rat

机译:小檗碱对百草枯诱导肝脏毒性的肝保护作用

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摘要

Paraquat (PQ) is a herbicide agent commonly used in agricultural applications. Hepatotoxicity is among clinical complications associated with PQ intoxication. Oxidative stress and its subsequent events are major mechanisms identified in PQ-induced liver toxicity. Berberine (BBR) is a natural antioxidant widely investigated for its hepatoprotective effects. The present study designed to evaluate the potential cytoprotective properties of BBR against PQ-induced cytotoxicity in primary cultured rat hepatocytes and in vivo test of liver function enzymes. Cellular and biochemical parameters including lactate dehydrogenase (LDH), cell viability, ROS formation, glutathione (GSH) content, and mitochondrial membrane potential in the PQ-treated hepatocytes were measured, and the mentioned markers were evaluated in the presence of BBR. BBR treatment caused significant decrease in PQ-induced cell death, ROS formation, and LDH release. On the other hand, it was found that BBR inhibits cellular glutathione depletion in PQ-treated hepatocytes. Also, BBR treatment significantly diminished PQ-induced the liver function enzyme elevation. These data mention the potential hepatoprotective effect of BBR with therapeutic capability against PQ-induced liver damage.
机译:百草枯(PQ)是常用于农业应用的除草剂。肝毒性是与PQ中毒相关的临床并发症。氧化应激及其随后的事件是PQ诱导的肝毒性中鉴定的主要机制。小檗碱(BBR)是一种自然抗氧化剂,广泛研究其肝脏保护作用。本研究旨在评估BBR对肝功能酶的初级培养大鼠肝细胞中PQ诱导的细胞毒性的潜在细胞毒性特性及对肝功能酶的体内试验。测量包括乳酸脱氢酶(LDH),细胞活力,ROS形成,谷胱甘肽(GSH)含量和线粒体膜电位的细胞和生化参数,并在BBR的存在下评价所述标记物。 BBR治疗引起PQ诱导的细胞死亡,ROS形成和LDH释放的显着降低。另一方面,发现BBR抑制PQ处理的肝细胞中的细胞谷胱甘肽枯萎病。此外,BBR处理显着降低PQ诱导肝功能酶升高。这些数据提到了BBR对PQ诱导的肝损伤的治疗能力的潜在的肝脏保护作用。

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