目的:研究慢性氟中毒大鼠肾脏过氧化损伤与细胞凋亡、自噬的相关性.方法:选择雄性SD大鼠作为实验动物并随机分为模型组和对照组,建立慢性氟中毒大鼠模型后检测血清中肾损伤标志物的含量以及肾脏组织中氧化应激损伤标志物的含量、细胞凋亡基因的表达量、细胞自噬基因的表达量.结果:造模后1个月、2个月、3个月时,模型组大鼠血清中BUN、Scr的含量均显著高于对照组,模型组大鼠肾脏组织中ROS的含量以及calpain-1、caspase-3、Notch1、Hes1mTOR、Beclin-1的mRNA表达量以及LC3-II/LC3-I的比例均显著高于对照组.Pearson检验显示:大鼠肾脏组织中ROS的含量与血清中BUN、Scr的含量以及肾脏组织中calpain-1、caspase-3、Notch1、Hes1mTOR、Beclin-1的mRNA表达量以及LC3-II/LC3-I的比例呈正相关.结论:慢性氟中毒大鼠过氧化所致肾脏损伤与细胞凋亡、自噬的过度激活密切相关.%Objective: To study the correlation between peroxidative damage and apoptosis, autophagy in rats with chronic fluorosis.Methods: Male SD rats were selected as experimental animal and randomly divided into model group and control group.After the establishment of chronic fluorosis, renal injury markers in serum and oxidative stress markers contents, apoptosis genes expression, autophagy gene expression in kidney tissue were determined.Results: One months, 2 months, 3 months after modeling, serum BUN and Scr contents model group were significantly higher than control group, ROS contents and calpain-1, Caspase-3, Notch1, Hes1, mTOR, Beclin-1 expression and LC3-II/LC3-I ratio in renal tissues were significantly higher than the control group.Pearson test showed that serum contents positively correlated with serum BUN, Scr contents and calpain-1, Caspase-3, Notch1, Hes1, mTOR, Beclin-1 expression and LC3-II/LC3-I ratio in renal tissues.Conclusions: The renal injury induced by chronic fluorosis in rats was closely related to the excessive activation of apoptosis and autophagy.
展开▼
