中文摘要：

目的观察凉血化瘀方对大鼠急性肝损伤的保护作用，并探讨其机制。方法SD健康雄性大鼠50只，随机分为正常对照组，D一氨基半乳糖（GalN）＋脂多糖（LPS）模型组，凉血化瘀方高、中、低剂量治疗组。末次给药后1h除正常组外其余4组按0．1midl0g腹腔注射D—GalN（50mg／mL）加LPS（0．48~tg／mL），造成大鼠急性肝损伤模型。用HE染色，观察肝组织病理变化；电镜观察肝细胞形态及结构；TUNEL法检测肝细胞凋亡；Westernblot检测细胞凋亡蛋白Caspase-9、Caspase-3、Bcl-2、Chop的表达情况。结果各剂量凉血化瘀方均改善肝组织病理损伤；凉血化瘀方各剂量组细胞凋亡蛋白Caspase-9、Caspase-3、Chop的表达下调（P均〈0．05或0．01），而抗凋亡蛋白Bcl-2表达上调，肝细胞形态改善明显。结论凉血化瘀方能抑制肝细胞凋亡。机制主要与调控线粒体和内质网应激途径诱导的细胞凋亡相关。

英文摘要：

Objective： To study the protection and the mechanism effect of Liangxuehuayu Decoction on the rats with acute liver injury. Methods： 50 SD rats were randomly divided into 5 groups.Each group except the normal group was injected 0.1 mL/10 g GaIN （50 mg/mL） and LPS（0.48 tLg/mL） to cause acute liver injury（ALI）. The pathological changes of hepatic tissue were observed by HE staining. Liver cell morphology and structure were observed with electron microscope. Meanwhile,the apoptosis of hepatic ceils were detected by TUNE method. Western blot was used to detect the apoptotic protein Caspase-9, Caspase-3, Bcl-2 and Chop. Results： Various doses of LHR were improved the liver lesion. In the treatment group,the expression of Caspase-9, Caspase-3 and Chop were down-regulated ,while the expression of Bcl-2 was up-regulated, and liver cell morphology was greatly improved. Conclusion： Liangxuehuayu Decoction could inhibit the apoptosis of hepatocytes. The major mecha- nisms were induced by protein expression on the apoptotic pathway of mitochondria stress and endoplasmic retic- ulum stress.