Protective effect of Echinochrome against intrahepatic cholestasis induced by alpha-naphthylisothiocyanate in rats
Protective effect of Echinochrome against intrahepatic cholestasis induced by alpha-naphthylisothiocyanate in rats
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DOI：
10.1590/1519-6984.192697
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发表时间：
2020-02-01
影响因子：
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通讯作者：
Aal, Wafaa E Abd-El
中科院分区：
文献类型：
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作者：
Fahmy, Sohair R;Sayed, Dawlat A;Aal, Wafaa E Abd-El
本研究旨在评估棘红花色 (Ech) 对单次 (i.p.) 注射 α-萘基异硫氰酸酯 (ANIT)（75 毫克/千克体重）诱导的大鼠肝内胆汁淤积的保护作用。给大鼠口服Ech（1、5和10mg/kg体重）或熊去氧胆酸（UDCA）80mg/kg体重药物预处理48小时（一剂/24小时），然后注射ANIT。注射ANIT后24h，血清丙氨酸氨基转氨酶(ALT)、天门冬氨酸氨基转氨酶(AST)和碱性磷酸酶(ALP)活性明显升高，并伴有胆管上皮细胞大量炎症。 ANIT还增加总蛋白(TP)、总胆红素(TB)、直接胆红素(DB)、间接胆红素(IB)的水平，但降低白蛋白含量(ALB)。此外，ANIT 增加肝脏 MDA 和 NO 水平，降低 GSH 水平和 GST 活性。通过显着降低血清 AST、ALT 和 ALP 活性以及 TP、TB、DB 和 TB 水平以及肝脏 MDA 水平和 NO 水平来评估 Ech 发挥保肝和抗胆汁淤积作用。总之，Ech被发现对ANIT等肝毒素引起的肝内胆汁淤积具有保肝作用。
The present study was designed to evaluate the protective effects of echinochrome (Ech) on intrahepatic cholestasis in rats induced by a single (i.p.) injection of alpha-naphthylisothiocyanate (ANIT) (75 mg/kg body weight). The rats were pre-treated orally for 48hr (one dose / 24hr) with Ech (1, 5 and 10 mg/kg body weight) or ursodeoxycholic acid (UDCA) 80 mg/kg body weight drug then, injected with ANIT. ANIT markedly increased serum activities of alanine amino transaminase (ALT), aspartate amino transaminase (AST) and alkaline phosphatase (ALP), which was accompanied by a massive inflammation of epithelial cells on bile duct at 24h after ANIT injection. ANIT also increased the levels of total protein (TP), total bilirubin (TB), direct bilirubin (DB), indirect bilirubin (IB), however decrease albumin content (ALB). In addition ANIT increased hepatic MDA and NO level and decreased GSH level and GST activity. The Ech exerted hepatoprotective and anticholestatic effects as assessed by a significant decrease in the activities of serum AST, ALT and ALP, and the levels of TP, TB, DB and TB as well as liver MDA level and NO level. In conclusion, Ech was found to possess hepatoprotective effect against intrahepatic cholestasis induced by hepatotoxin such as ANIT.