摘要
目的探讨丙酮酸乙酯(EP)对D-氨基半乳糖所致的大鼠急性肝损伤的保护作用及其可能机制。方法采用D-氨基半乳糖复制急性肝损伤(ALI)模型,Wistar大鼠随机分为正常对照组、ALI组、EP干预组。用Westernblot方法测定肝组织高迁移率族蛋白B1(HMGB1),鲎实验法检测血清中内毒素水平,全自动生化分析仪测定肝功能指标。结果与正常对照组相比,ALI后24～72hHMGB1表达显著升高(P<0.01);血清内毒素水平逐渐升高,24h达到高峰;血清丙氨酸转氨酶(ALT)6h和24h有两个峰值,且24h峰值高于6h。与ALI组相比,EP干预组24～72hHMGB1蛋白表达均显著抑制(P<0.01),内毒素和ALT在24、48、72h也均有不同程度下降(P<0.05)。结论EP可减轻D-氨基半乳糖所致的ALI。其机制可能是EP下调了肝组织中HMGB1蛋白表达和降低血清中的肠源性内毒素水平。
Objective To study the protective effects of ethyl pyruvate（EP）on acute hepatic failure （ALI） in rats. Methods Ninety wistar rats were randomly divided into three groups： ALI group（n=30）： rats with ALI were in-dueed by injecting D-GaIN intraperitoneally. EP group （n=30）： rats were administered ethyl pyruvate 1 h before ALI. Normal group （n=30）： rats were administered Ringer＇s solution. Six animals in each group were sacrificed in different time points, then their sera as well as hepatic tissues were collected to determine ALT and LPS （ lipopolysaccharide ） levels and HMGB1 （ high mobility group box 1 ） expression. Results Compared with normal group, HMGB1 expression were significantly increased in the.liver during 24-72 h after ALI （ P〈0.01 ）, and serum ALT and LPS were significantly elevated （ P〈0.01 ）. In EP group, HMGB1 expression in the liver were markedly decreased during 24-72 h, compared with ALl group, serum ALT and LPS levels were markedly reduced during 24-72 h after ALl. Conelusion EP could significandy reduce HMGB1 release in the liver and decrease serum LPS level. So EP could provide partly protection against liver injury.
出处
《中国药物与临床》
CAS
2006年第10期739-741,共3页
Chinese Remedies & Clinics
