益气活血方介导P38MARK信号转导通路促进腰椎间盘突出重吸收的机制

After lumbar disc protrusion shrink or disappear phenomenon, called the intervertebral disc heavy absorption.The discovery of this phenomenon for the non-surgical treatment of lumbar disc prolapse gives a new exploration direction.Among them, promote disc herniation after heavy absorption of Chinese medicine research at present, both at home and abroad is still a gap, is one of the direction of worth exploring.New blood vessels ingrowth and inflammatory reaction is to promote recognized mechanism of disc herniation after heavy absorption.Based on p38MAPK signal transduction pathway in the human body cell apoptosis and cellular structure reconstruction have important role, and the path can be through the new blood vessels inflammatory reaction after the ingrowth is activated, we speculated that the pathway in disc herniation after heavy absorption may play a very important role.Our previous study by establishing the rat intervertebral disc heavy absorption model and clinical observe called simply MRl, confirmed the yiqi huoxue can promote disc herniation after heavy absorption.This topic proposed in previous research, on the basis of further research: (1) p38 lightning MAPK signal transduction pathway of intervertebral disc herniation after heavy absorption effect;(2) whether yiqi huoxue fang by p38 lightning MAPK signal transduction pathway plays a role of promoting heavy absorption after lumbar disc.Aiming at traditional Chinese medicine treatment of fracture type lumbar intervertebral disc protrusion is safe and effective to provide science.

腰椎间盘突出后，突出物发生变小或消失的现象，称为突出椎间盘的重吸收。此现象的发现，为腰椎间盘突出症的非手术治疗赋予了新的研究方向。但迄今为止，中医药促进椎间盘突出后的重吸收研究,仍是国内外的空白点，迫待深入探索。目前认为，新生血管长入突出椎间盘引发炎性反应是发生重吸收的重要机制。基于p38MAPK信号通路在人体细胞凋亡及细胞结构重构方面有重要的作用，且该通路可通过新生血管长入后的炎性反应而激活，我们推测该通路在椎间盘突出后的重吸收机制中可能发挥重要的作用。我们前期研究通过建立大鼠腰椎间盘突出模型观察及临床病例MRl随访比较，证实了益气活血方能促进突出椎间盘的重吸收。本课题拟在此基础上，进一步研究：（1）p38 MAPK信号转导通路对椎间盘突出后重吸收的影响；（2）益气活血方是否通过p38 MAPK信号转导通路达到促进腰椎间盘突出后重吸收的作用，旨在为中医药治疗腰椎间盘突出症提供科学依据。

腰椎间盘突出后重吸收现象的发现，为腰椎间盘突出症的非手术治疗赋予了新的研究方向。目前认为，新生血管长入突出椎间盘引发炎性反应是发生重吸收的重要机制。基于 p38MAPK 信号通路在人体细胞凋亡及细胞结构重构方面有重要的作用，且该通路可通过新生血管长入后的炎性反应而激活，我们推测该通路在椎间盘突出后的重吸收机制中可能发挥重要的作用。我们前期研究通过建立大鼠腰椎间盘突出模型观察及临床病例 MRl 随访比较，证实了益气活血方能促进突出椎间盘的重吸收。.本研究通过建立破裂型腰椎间盘突出动物模型及体外实验模型，采用 P38 MAPK阻断剂和中药益气活血方交互干预后，观察大鼠椎间盘质量、体积、HE染色形态学的变化以及重要因子VEGF、TNF-α、IL-1 及P38MAPK、P-p38MAPK等的表达，探讨P38MAPK信号通路在重吸收过程中的作用及益气活血方是否通过该通路影响重吸收的发生。.实验结果发现P38 MAPK信号通路被阻断后椎间盘中炎症因子TNF-α、IL-1、VEGF和 P-p38的表达皆有下降，椎间盘质量及体积下降的趋势被弱化，可见P38 MAPK通路被阻断后椎间盘重吸收趋势被弱化，因此P38 MAPK信号通路在重吸收过程中具有重要作用。而益气活血方干预后 TNF-α、IL-1、VEGF、P-p38MAPK的 mRNA和蛋白表达水平都高于空白对照组，这表明益气活血方可以通过促进新生血管长入椎间盘，炎性因子不断产生并聚集，激活P38 MAPK信号通路，进而促进重吸收的发生发展。.本项目证实益气活血方可通过激活p38 MAPK 信号转导通路促进突出椎间盘出现重吸收，为中医药治疗腰椎间盘突出症提供理论依据。