Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats

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

您当前的位置：

首页 >

文章列表页 >

Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats

更新时间：2026-01-09

- Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats
- Journal of Army Medical University Vol. 37, Issue 17, Pages: 1744-1749(2015)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：
  CLC： R392.3;R711.32;R992
- Published：2015
- 稿件说明：
移动端阅览
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.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].陆军军医大学学报(原第三军医大学学报),2015,37(17):1744-1749.

　Liao Xinggui,Li Yanli,Qiu Yiwen,Zhou Yongjiang,Geng Yanqing,Liu Xueqing,Chen Xuemei,Wang Yingxiong,He Junlin.Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(17):1744-1749.
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.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].陆军军医大学学报(原第三军医大学学报),2015,37(17):1744-1749. DOI：

　Liao Xinggui,Li Yanli,Qiu Yiwen,Zhou Yongjiang,Geng Yanqing,Liu Xueqing,Chen Xuemei,Wang Yingxiong,He Junlin.Sodium fluoride activates P38 and JNK via induction of oxidative stress to promote uterine inflammation in rats[J].J Amry Med Univ (J Third Mil Med Univ),2015,37(17):1744-1749. DOI：

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（P0.05）；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（P0.05）；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（P0.05），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 (P0.05). 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 (P0.05). 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.

关键词

Keywords

references

Views

下载量

CSCD

Alert me when the article has been cited

提交

Tools

Publicity Resources

NLRP3 inflammasome activation mediates terahertz exposure-induced skin aseptic inflammation in mice

Predictive value of serum heme oxygenase-1 and C-reactive protein for coronary artery lesions in children with Kawasaki disease: report of 89 cases

Effect of cobalt protoporphyrin-induced heme oxygenase 1 un-regulation on oxidative stress and inflammatory responses in skeletal muscle of aged mice

Role and mechanism of SIRT3 in oxidative stress and mitochondrial biogenesis in alveolar type II cells

p300 promotes hepatic lipid accumulation in dyslipidemia by regulating SREBP-1c acetylation

Related Author

高鹏

卢永辉

马秦龙

李敏

陈纯海

何旻蒂

余争平

何先凤

Related Institution

Department of Human Anatomy， Anhui Medical University

Laboratory of Stem Cell and Tissue Engineering， Chongqing Medical University

Institute of Field Surgery， Daping Hospital， Army Medical University

Department of Geriatrics and Special Service Medicine， First Affiliated Hospital（Southwest Hospital）， Army Medical University （Third Military Medical University）

达州市中西医结合医院药学科

⁰