电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆

袁爱红; 曹江鹏; 杨骏; 宋小鸽; 查必祥; 高志群; 叶敏

doi:10.13702/j.1000-0607.190870

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电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆

机制探讨 | 更新时间：2023-08-11

- 电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆
- Electroacupuncture improves learning-memory ability in diabetic rats with cognitive impairment via inhabitating proinflammatory cytokine production through p38 MAPK and STAT3 pathway
- 针刺研究 2020年45卷第8期页码：603-610
- 作者机构：
  
  1. 安徽中医药大学第一附属医院
  2. 安徽中医药大学研究生院
  3. 安徽中医药大学针灸经络研究所
- 作者简介：
- 基金信息：
  
  国家自然科学基金项目(No.81202769);全国名老中医药专家杨骏传承工作室项目;2016-2018年安徽高校科研创新平台团队项目(No.2015TD033)
- DOI：10.13702/j.1000-0607.190870
  中图分类号：
- 纸质出版日期：2020
- 稿件说明：
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袁爱红, 曹江鹏, 杨骏, 等. 电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆[J]. 针刺研究, 2020,45(8):603-610.

YUAN Ai-hong, CAO Jiang-peng, YANG Jun, et al. Electroacupuncture improves learning-memory ability in diabetic rats with cognitive impairment via inhabitating proinflammatory cytokine production through p38 MAPK and STAT3 pathway[J]. Acupuncture research, 2020, 45(8): 603-610.
袁爱红, 曹江鹏, 杨骏, 等. 电针通过p38 MAPK和STAT3信号通路抑制糖尿病认知障碍大鼠促炎性细胞因子生成改善学习记忆[J]. 针刺研究, 2020,45(8):603-610. DOI： 10.13702/j.1000-0607.190870.

YUAN Ai-hong, CAO Jiang-peng, YANG Jun, et al. Electroacupuncture improves learning-memory ability in diabetic rats with cognitive impairment via inhabitating proinflammatory cytokine production through p38 MAPK and STAT3 pathway[J]. Acupuncture research, 2020, 45(8): 603-610. DOI： 10.13702/j.1000-0607.190870.

摘要

目的:观察电针对糖尿病认知障碍大鼠海马及前额叶皮层细胞因子的影响

探讨p38丝裂原活化蛋白激酶(p38 MAPK)和信号转导及转录激活子3(STAT3)在电针改善学习记忆中的作用。方法:SD大鼠随机分为正常组10只

造模组90只

造模组大鼠以高脂高糖饲料喂养1个月后

采用小剂量链脲佐菌素腹腔注射法建立糖尿病模型。通过Morris水迷宫实验筛选出糖尿病模型大鼠中出现认知障碍的大鼠20只

随机分为模型组和电针组各10只。电针组大鼠予针刺"后三里""内庭"及"胰俞"

其中"后三里"和"内庭"予以电针干预

每周6次

每次20 min

连续治疗4周。针刺干预结束后

检测各组大鼠随机血糖值;应用Morris水迷宫实验测定大鼠学习与记忆能力;采用Western blot及实时荧光定量PCR法检测各组大鼠海马及前额叶皮层中白细胞介素(IL)-6、IL-1β、肿瘤坏死因子(TNF)-α、p38 MAPK、磷酸化(p)-p38 MAPK、STAT3和p-STAT3蛋白及mRNA相对表达量;采用免疫荧光法检测各组大鼠海马及前额叶皮层中p38 MAPK和STAT3表达。结果:实验结束时

模型组大鼠随机血糖值较正常组明显升高(P<0.001);与模型组比较

电针组大鼠随机血糖值明显降低(P<0.05)。模型组大鼠较正常组大鼠水迷宫逃避潜伏期明显延长(P<0.01);与模型组比较

电针组大鼠水迷宫逃避潜伏期明显缩短(P<0.05)。模型组大鼠海马及前额叶皮层IL-6、IL-1β、TNF-α、p38 MAPK、p-p38 MAPK、STAT3和p-STAT3蛋白及mRNA表达较正常组明显升高(P<0.001);与模型组比较

电针组大鼠海马及前额叶皮层IL-6、IL-1β、TNF-α、p38 MAPK、p-p38 MAPK、STAT3和p-STAT3蛋白及mRNA表达明显降低(P<0.001)。模型组大鼠海马及前额叶皮层中p38 MAPK和STAT3的平均荧光强度值明显高于正常组(P<0.001);与模型组比较

电针组大鼠海马及前额叶皮层中p38 MAPK、STAT3的平均荧光强度值明显降低(P<0.001

P<0.05)。结论:电针可以抑制糖尿病认知障碍大鼠海马和前额叶皮层中促炎性细胞因子的过量产生

p38 MAPK和STAT3信号通路可能参与其中。

Abstract

Objective To investigate the effect of electroacupuncture(EA) on the p38 mitogen-activated protein kinase(p38 MAPK) and signal transducer and activator of transcription 3(STAT3) pathway in hippocampus and frontal cortex of diabetic rats with cognitive impairment(CI)

as well as the mechanism of EA in protection against CI in diabetic rats. Methods Thirty SD rats were divided into normal

model and EA groups(n=10 rats/group). The diabetic model was established by i.p.injection of Streptozotocin solution(25 mg/kg)

followed by high-fat diet raising for 1 month

and the CI rats was confirmed by Morris water maze tasks. The rats in the EA group were given acupuncture at "Zusanli"(ST36) "Neiting"(ST44) and "Yishu"(EX-B3) 20 min/d

among which ST36 and ST44 were treated with EA. The treatment was conducted 6 times a week for 4 weeks. The fasting blood glucose(FBG) contents were assayed by glucometer before and after treatment. The rats' learning-memory ability was detected by Morris water maze tasks. The expression levels of IL-6、IL-1β、TNF-α、p38 MAPK、p-p38 MAPK、STAT3 and p-STAT3 in hippocampus and frontal cortex were detected by Western blot and quantitative real-time PCR

separately. The mean fluorescence intensity of p38 MAPK and STAT3 was observed by immunofluorescence histochemistry. Results After modeling

FBG and the escape latency of Morris water maze tasks were significantly increased in the model group compared with the normal group(P<0.001

P<0.01). Following EA treatment

the increased FBG and average escape latency were markedly reversed in the EA group relevant to the model group(P<0.05). Compared with the normal group

the proteins and mRNAs expression of IL-6

IL-1β

TNF-α

p38 MAPK

p-p38 MAPK

STAT3 and p-STAT3 in hippocampus and frontal cortex were significantly increased in the model group(P<0.001)

as well as the mean fluorescence intensity of p38 MAPK and STAT3 in hippocampus and frontal cortex(P<0.001). Following EA intervention

the proteins and mRNAs expression of IL-6

IL-1β

TNF-α

p38 MAPK

p-p38 MAPK

STAT3 and p-STAT3

and the mean fluorescence intensity of p38 MAPK and STAT3 in hippocampus and frontal cortex were down-regulated(P<0.001

P<0.05). Conclusion EA can inhibit the over production of pro-inflammatory cytokines in diabetic rats with CI

possibly by regulating the expression of p38 MAPK and STAT3 pathway.

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