论文部分内容阅读
目的:研究莲心总碱(TAENN)对脂多糖和D-氨基半乳糖(LPS/GalN)诱导小鼠急性肝衰竭肝脏的保护作用及可能作用机制。方法:昆明种雄性小鼠随机分为4组:正常对照组、模型组、TAENN高剂量组(100 mg·kg-1)、TAENN低剂量组(30 mg·kg~(-1))。腹腔注射LPS/GalN建立小鼠急性肝衰竭模型;通过生存曲线分析、HE组织化学染色、肝脏指数和血清转氨酶活性分析评价动物肝损伤程度;通过检测血清及肝脏内中SOD、GSH、MDA、ROS、CAT、GSH-Px水平评价小鼠整体和肝脏内氧化应激的状况。结果:口服TAENN能有效降低LPS/GalN诱导的小鼠死亡,HE染色观察显示TAENN能明显减轻LPS/GalN诱导的肝脏显微结构变化;此外,TAENN明显缓解了LPS/GalN诱导的肝脏肿大,降低了小鼠血清中ALT和AST活性水平(P<0.01)。进一步研究表明,TAENN明显降低了模型小鼠血清中MDA的含量,而血清GSH和SOD水平则明显增加(P<0.01);经TAENN处理后,小鼠肝组织中ROS和MDA的相对含量降低,而肝脏GSH、SOD、CAT和GSHPx水平则显著增加(P<0.01)。结论:TAENN能有效缓解LPS/GalN诱导的小鼠肝衰竭,且这种对肝脏的保护作用与其抑制LPS/GalN诱导的肝脏氧化应激相关。
Objective: To study the protective effect of lotus root base alkaloids (TAENN) on the liver of mice with acute liver failure induced by lipopolysaccharide and D-galactosamine (LPS / GalN) and its possible mechanism. Methods: Kunming male mice were randomly divided into 4 groups: normal control group, model group, TAENN high dose group (100 mg · kg -1) and TAENN low dose group (30 mg · kg -1). The model of acute liver failure was established by intraperitoneal injection of LPS / GalN. The liver injury was assessed by survival curve analysis, HE staining, liver index and serum aminotransferase activity. The levels of SOD, GSH, MDA and ROS in serum and liver , CAT, GSH-Px levels in mice as a whole and the situation of liver oxidative stress. RESULTS: Oral administration of TAENN effectively reduced the death of mice induced by LPS / GalN. HE staining showed that TAENN significantly reduced the changes of liver microstructure induced by LPS / GalN. In addition, TAENN significantly alleviated LPS / GalN-induced liver enlargement, Reduced the levels of ALT and AST in mouse serum (P <0.01). Further studies showed that TAENN significantly reduced MDA content in serum and serum GSH and SOD levels significantly (P <0.01). After TAENN treatment, the relative content of ROS and MDA in liver decreased, The liver GSH, SOD, CAT and GSHPx levels were significantly increased (P <0.01). CONCLUSION: TAENN can effectively relieve LPS / GalN-induced liver failure in mice, and this protective effect on the liver is related to its inhibition of LPS / GalN-induced hepatic oxidative stress.