氟化钠诱导氧化应激促进大鼠子宫组织炎症反应及其作用机制的初步研究.docVIP

DOI: 10.16016/j.1000-5404.201412236 氟化钠诱导氧化应激促进大鼠子宫组织炎症反应及其作用机制的初步研究 廖星贵，李艳丽，邱义稳，周永江，耿艳清，刘学庆，陈雪梅，王应雄，何俊琳 (400016 重庆，重庆医科大学公共卫生与管理学院生殖生物学研究室) 【摘要】目的 通过对氟化钠染毒大鼠的炎症反应相关因子及关键信号通路分子的检测，探讨其对大鼠子宫组织细胞氧化损伤的作用机制。方法 将30只雌性SD成年大鼠分为3组（10只/组），分别给予蒸馏水（对照组）、100mg/L氟化钠溶液（100mg/L氟化钠处理组）、200mg/L氟化钠溶液（200mg/L氟化钠处理组）饮用，持续染毒180d，建立氟化钠染毒动物模型。采用Western blot、免疫组织化学法检测子宫组织炎症相关因子Cox2、ICAM-1、TNF-α、IL-1β表达；采用ELISA法对氧化应激相关分子ROS、MDA、SOD、CAT、GSH进行检测；采用Western blot法测定P38、ERK、JNK、PI3K活性物质的表达。结果 2个氟化钠处理组大鼠子宫组织炎症相关因子Cox2、ICAM-1、TNF-α、IL-1β表达量明显高于对照组（P＜0.05）；处理组ROS、SOD、CAT、GSH明显高于对照组，而MDA明显低于对照组（P＜0.05）；与对照组相比，处理组P38、JNK蛋白磷酸化效率增加，而且ERK、PI3K总蛋白及磷酸化蛋白表达水平均有增加。结论 氟化钠可诱导大鼠子宫组织的氧化应激促进炎症反应发生，MAPK(ERK、JNK、P38)和PI3K信号通路可能参与其中。 【关键词】氟化钠，氧化应激，P38、JNK信号通路，子宫组织，炎症反应 【中图法分类号】 【文献标志码】A Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote inflammation of endometrium in rats Liao Xinggui， Qiu Yiwen， Zhou Yongjiang， Geng Yanqing， Liu Xueqing， Chen Xuemei， Wang Yingxiong， He Junlin （Laboratory of Reproductive Biology, School of Public Health, Chongqing Medical University, Chongqing, 400016，China） 【Abstract】Objective To investigate the mechanism of oxidative damage caused by NaF through the detection of inflammation-related factors and pathways on rats. Methods Sodium fluoride infected model was set up as following. 30 adult female SD rats which had no difference in age and weight were randomly divided into 3 groups (10 in each group), and were feeded for 180 days with pure water (control group), 100mg/L NaF (100mg/L NaF treated group) and 200mg/L NaF (200mg/L NaF treated group) respectively. Inflammation-related factors Cox2, ICAM-1, TNF-α,IL-1βwere measured by Western blot and immunohistochemistry, oxidative stress-related factors ROS、MDA、SOD、CAT、GSH were detected by ELISA, P38, ERK, JNK, PI3K pathway molecular were detected by Western blot. Results Endometrium of rats exposed to sodium fluoride had high expression of Cox2, ICAM-1, TNF-αand IL-1β（P＜0.05）. The level of