摘要
目的:探究竹节参多糖对LPS/D-GalN诱导急性肝损伤小鼠的保护作用及其机制。方法:采用腹腔注射LPS(8μg/kg)和D-GalN(800 mg/kg)诱导小鼠急性肝损伤。记录小鼠死亡时间并绘制生存曲线和计算肝脏指数并观察肝脏组织病理学变化,检测动物血清中肝脏酶水平以及肝匀浆中氧化应激因子和炎症因子,评价竹节参多糖对小鼠急性肝损伤的保护作用。结果:竹节参多糖能剂量依赖性地降低LPS/D-GalN诱导的肝损伤并提高肝损伤型动物在24 h内的生存率,剂量依赖性缓解肝脏病变。经竹节参多糖给药处理后,模型动物肝组织SOD、GSH活性升高,MDA、TNF-α、IL-1β和IL-6及血清ALT、AST均降低。结论:竹节参多糖能减轻LPS/D-GalN诱导的小鼠急性肝损伤,其作用机制可能与降低氧化应激和缓解炎症反应有关。
Objective: To study the protective effects and mechanism of total polysaccharides from Panax japonicus(PSPJ) on mice with acute liver injury induced by lipopolysaccharide and D-galactosamine(LPS/D-GalN).Methods: Acute liver injury was induced by intraperitoneal injection of LPS(8 μg/kg) and D-GalN(800 mg/kg).The survival curve was plotted by the time of death,and the liver indexes,and the liver histopathological changes were determined.Meanwhile,the levels of hepatic enzymes in serum,the levels of oxidative stress factor and inflammatory factor in liver homogenate were also determined,to evaluate the protective effects of PSPJ on acute liver injury in mice.Results: PSPJ alleviated LPS/GalN-induced acute liver injury and increased the survival rate of mice in the model group in 24 h in a dose-dependent manner and dose-dependently alleviate LPS/D-GalN-induced liver injury.In response to PSPJ administration,the activities of SOD and GSH in intra hepatic were increased,while the content of MDA,TNF-α,IL-1β and IL-6 in intra hepatic and ALT,AST in serum were declined.Conclusion: PSPJ can relieve LPS/D-GalN-induced acute liver injury in mice.Decreasing oxidative stress and relieving inflammatory responses are implicated in the liver protective activity of PSPJ.
出处
《中药材》
CAS
北大核心
2017年第5期1170-1173,共4页
Journal of Chinese Medicinal Materials
基金
国家科技部"十二五"科技支撑计划资助项目(2012BAI27B06)
国家自然科学基金(81073147)
关键词
竹节参多糖
肝损伤
氧化应激
炎症反应
Total polysaccharides from Panax japonicus
Liver injury
Oxidative stress
Inflammatory responses