[1]廖星贵,李艳丽,邱义稳,等.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[J].第三军医大学学报,2015,37(17):1744-1749.
 Liao Xinggui,Li Yanli,Qiu Yiwen,et al.Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats[J].J Third Mil Med Univ,2015,37(17):1744-1749.
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《第三军医大学学报》[ISSN:1000-5404/CN:51-1095/R]

卷:
37卷
期数:
2015年第17期
页码:
1744-1749
栏目:
论著
出版日期:
2015-09-15

文章信息/Info

Title:
Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats
作者:
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
重庆医科大学公共卫生与管理学院生殖生物学研究室
Author(s):
Liao Xinggui Li Yanli Qiu Yiwen Zhou Yongjiang Geng Yanqing Liu Xueqing Chen Xuemei Wang Yingxiong He Junlin

Laboratory of Reproductive Biology, School of Public Health and Management, Chongqing Medical University, Chongqing, 400016, China

关键词:
氟化钠氧化应激P38JNK信号通路子宫炎症反应
Keywords:
sodium fluoride oxidative stress P38 JNK signaling pathway uterus inflammation
分类号:
R392.3; R711.32; R992
文献标志码:
A
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)、100 mg/L氟化钠溶液(100 mg/L氟化钠处理组)、200 mg/L氟化钠溶液(200 mg/L 氟化钠处理组)饮用,持续染毒180 d,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Cox-2、ICAM-1、TNF-α、IL-1β表达;采用ELISA对氧化应激相关分子ROS、MDA、SOD、CAT、GSH进行检测;采用Western blot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Cox-2、ICAM-1、TNF-α、IL-1β表达量明显高于对照组(P<0.05);2个氟化钠处理组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,2个氟化钠处理组P38、JNK蛋白磷酸化效率增加(P<0.05),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。

Abstract:

Objective       To investigate the mechanism of oxidative damage caused by sodium fluoride (NaF) through detecting inflammation-related factors and signaling pathway molecules in rats.       Methods       NaF poisoning model was established. Thirty adult female SD rats, which had no difference in age and weight, were randomly divided into 3 groups (10 in each group), and then fed with pure water (control group), 100 mg/L NaF (100 mg/L NaF-exposed group) and 200 mg/L NaF (200 mg/L NaF-exposed group), respectively, for 180 days. Inflammation-related factors Cox-2, ICAM-1, TNF-α and IL-1β were measured by Western blotting and immunohistochemistry, and oxidative stress-related factors ROS, MDA, SOD, CAT and GSH were detected by ELISA. In addition, signaling pathway molecules P38, ERK, JNK and PI3K were analyzed by Western blot.       Results       Cox-2, ICAM-1, TNF-α and IL-1β were highly expressed in the endometria of the rats exposed to NaF (P<0.05). The levels of ROS, SOD, CAT and GSH were higher in the NaF-exposed groups, but the MDA level was lower compared with the control group (P<0.05). In the NaF-exposed groups, phosphorylation levels of P38 and JNK were significantly increased. Though ERK and PI3K proteins and their phosphorylation levels were also increased in the NaF-exposed groups, there was no significant difference between the NaF-exposed groups and the control group.       Conclusion       NaF activates P38 and JNK via induction of oxidative stress to promote inflammation of the endometria in the rats.

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更新日期/Last Update: 2015-09-07