HMGB1介导的炎症通路在雷公藤致大鼠肝损伤中的作用研究-中国药房

HMGB1介导的炎症通路在雷公藤致大鼠肝损伤中的作用研究

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篇名：	HMGB1介导的炎症通路在雷公藤致大鼠肝损伤中的作用研究
TITLE：
摘要：	目的：研究高迁移率族蛋白B1（HMGB1）介导的炎症通路HMGB1-Toll样受体4（TLR4）/核转录因子κB（NF-κB）在雷公藤致大鼠肝损伤中的作用，为阐明雷公藤致肝损伤的作用机制提供参考。方法：将24只SD大鼠随机分为空白组（生理盐水，灌胃）、雷公藤组（以生药计16 g/kg，灌胃）和中和剂组（腹腔注射100 mg/kg甘草酸铵溶液3 h后再灌胃以生药计16 g/kg的雷公藤），每组8只，各组大鼠均连续给药3周。每周给药后均检测大鼠血清中天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）水平；给药结束后，采用酶联免疫吸附法检测大鼠血清中HMGB1、白细胞介素1β（IL-1β）、IL-2、肿瘤坏死因子α（TNF-α）水平，Western blot法检测大鼠肝组织中HMGB1、NF-κB p65、TLR4蛋白表达，苏木精-伊红染色后观察大鼠肝组织病理学改变。结果：给药3周后，雷公藤组大鼠血清中AST、ALT、HMGB1、IL-1β、IL-2、TNF-α水平以及肝组织中HMGB1、NF-κB p65、TLR4蛋白表达水平均显著高于空白组和中和剂组（P＜0.05或P＜0.01）。雷公藤组大鼠肝组织中央静脉周围肝细胞水肿，部分肝细胞浆内可见圆形空泡；中和剂组大鼠仅少量细胞内可见大小不一的空泡。结论：雷公藤致大鼠肝损伤的机制可能与其激活了HMGB1-TLR4/NF-κB炎症通路有关。
ABSTRACT：	OBJECTIVE： To study the effects of high-mobility group box 1 protein （HMGB1）-mediated inflammatory pathway HMGB1-Toll like receptor 4 （TLR4）/nuclear transcription factor κB（NF-κB）on liver injury of rats induced by Tripterygium wilfordii， and to provide reference for clarify the mechanism of liver injury induced by T. wilfordii. METHODS： Totally 24 SD rats were randomly divided into blank group （normal saline， i.g.）， T. wilfordii group （16 g/kg by crude drug， i.g.） and neutralizer group （16 g/kg T. wilfordii crude drug i.g. after i.p injection of 100 mg/kg Ammonium glycyrrhizinate solution 3 h）， with 8 rats in each group. All rats were treated for consecutive 3 weeks. The serum levels of AST and ALT in rats were detected every week. After the end of medication， the serum levels of HMGB1， IL-1β， IL-2 and TNF-α were detected by ELISA method； the protein expression of HMGB1， NF-κB p65 and TLR4 in liver tissue of rats were detected by Western blot assay. The pathological changes of liver tissue in rats were measured with HE staining method. RESULTS： After 3 weeks of treatment， the serum levels of AST， ALT， HMGB1， IL-1β， IL-2 and TNF-α in rats， the protein expression of HMGB1， NF-κB p65 and TLR4 in liver tissue of rats in T. wilfordii group were significantly higher than blank group and neutralizer group （P＜0.05 or P＜0.01）. Hepatocyte edema was found around the central vein of the liver， and circular vacuoles were seen in some hepatic cytoplasm in T. wilfordii group； only varying size of vacuoles were found in a small number of cells in neutralizer group. CONCLUSIONS： T. wilfordii induced liver injury may be associated with the activation of HMGB1-TLR4/NF-κB inflammation pathway.
期刊：	2018年第29卷第5期
作者：	董捷鸣，章从恩，于小红，吴昊，马致洁，赵奎君
AUTHORS：	DONG Jieming，ZHANG Cong’en，YU Xiaohong，WU Hao，MA Zhijie，ZHAO Kuijun
关键字：	雷公藤；肝损伤；高迁移率族蛋白1；Toll样受体4；核转录因子κB；大鼠
KEYWORDS：	Tripterygium wilfordii； Liver injury； High-mobility group box 1 protein； Toll like receptor 4； Nuclear transcription factor κB； Rats
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