摘要
为研究内毒素(ET)诱导肝细胞凋亡的作用机制及阳离子A(CA)对肝细胞的保护效应,采用ET所致家兔内毒素休克的模型,分别在3、4、81、2 h检测肝脏组织中一氧化氮(NO)水平的动态变化、肝细胞凋亡指数和肝细胞凋亡的形态学变化,并观察CA注射液对上述指标的影响。ET组中各时间段的肝组织中NO水平均显著升高(P<0.01),随着NO水平的增加,肝细胞凋亡指数先上升,然后下降,最后又上升到最高值;肝细胞及肝脏组织的损害程度也与此类似。CA组的NO水平则明显降低(P<0.05),肝细胞凋亡及病理组织学改变亦轻。提示NO参与内毒素休克的发病机制,介导了肝细胞的凋亡,同时,在一定范围内又有保肝作用。而CA可有效地中和血循环中的ET,减少肝脏中过量NO的产生,减轻炎症反应及其对肝脏的损害,对内毒素休克有一定的防治作用。
To investigate the apoptosis mechanism of hepatocyte induced by endotoxin（ET） and protective effect of Cation A （CA）, the nitric oxide （NO） levels of liver tissue and the percentage of apoptosis of hepatocyte were measured 3,4,8,12 h post treatment respectively in the normal control group, ET group and CA protective group. The NO levels of all detected times were increased markedly in ET group （P〈0.01）, the percentage of apoptosis of hepatocyte displayed three periods, increased, decreased and increased, which were confirmed pathologically with obvious damage of cells and tissue of liver. While in CA group the above mentioned parameters and damage of cells and tissue of liver were reduced significantly （P〈0.01, P〈0.05）. Results showed that NO might be involved in pathogenesis of endotoxic shock, primarily through the induction of hepatocytes apoptosis, and CA could be used in preventing or treating it by mechanism of effectively reducing ET-induced production of inflammatory factors and massive NO of liver.
出处
《畜牧兽医学报》
CAS
CSCD
北大核心
2006年第1期61-64,共4页
ACTA VETERINARIA ET ZOOTECHNICA SINICA
基金
国家自然科学基金项目(30360079)
教育部高等学校骨干教师资助计划(教计司[2000]65号)资助
