Tuina alleviates the muscle atrophy of sciatic nerve injury rats through regulating PI3K/Akt signaling

Author:

张 英奇1,张 羽羽1,刘 嘉悦1,周日 佳伟1,徐 岳1,shi Narentuya1,张 洪正1,燕 嘉旺1,陈 金平1,王 Hourong2,余 天源1

Affiliation:

1. Beijing University of Chinese Medicine

2. Beijing Hospital

Abstract

Abstract

Background Tuina has been shown to be an effective treatment for the decrease of skeletal muscle atrophy after Peripheral nerve injury (PNI). However, its mechanism is unclear. This study aimed to explore the underlying mechanisms of tuina on rats with sciatic nerve injury (SNI). Methods A rat model of SNI was established. After a total of 20 times tuina intervention, the curative effects were evaluated by behavioral assessment, nerve function index and muscle atrophy index (MAI). The pathological changes were observed by transmission electron microscopy and immunofluorescence. The levels of IGF-1 and FoxO were detected by enzyme-linked immunosorbent assay (ELISA). Western blotting was used to detect the expression of proteins in the PI3K/AKT signaling pathway. Result The behavioral assessment, nerve function index and MAI proved that tuina significantly improved muscle atrophy after SNI compared with that in SNI model group. Transmission electron microscopy showed that tuina improved ultramicrostructure and immunofluorescence of CD31 showed that tuina improved microcirculation. Further, we observed that tuina differentially regulated levels of IGF-1 and FoxO and the protein expression of p-PI3K, p-AKT and VEGF in anterior tibial muscle and soleus muscle. Conclusion Tuina could effectively inhibit skeletal muscle atrophy via the microcirculation pathway in the rat model of SNI, by regulating the expression levels of IGF-1, FoxO. The underlying mechanism of action might be via the PI3K/Akt signaling pathway.

Publisher

Springer Science and Business Media LLC

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3