Role of p38 MAPK Pathway in Diabetic Peripheral Neuropathy and Chinese Medicine Intervention： A Review
10.13422/j.cnki.syfjx.20230725
- VernacularTitle:p38 MAPK通路在糖尿病周围神经病变中的作用及中药干预的研究进展
- Author:
Peng YANG
1
;
Chengfei ZHANG
2
;
Yaqi ZHANG
3
;
Chuan PENG
4
;
Qiue ZHANG
2
;
Lili WU
2
;
Lingling QIN
2
;
Tonghua LIU
2
;
Xiaohong MU
3
Author Information
1. The First Clinical School of Medicine， Shaanxi University of Chinese Medicine， Xianyang 712046， China
2. Key Laboratory of Traditional Chinese Medicine （TCM） and Health Sciences， Ministry of Education， Beijing University of Chinese Medicine， Beijing 100029， China
3. Dongzhimen Hospital， Beijing University of Chinese Medicine， Beijing 100700， China
4. Chengdu University of TCM， Chengdu 610075， China
- Publication Type:Journal Article
- Keywords:
diabetic peripheral neuropathy;
inflammation;
oxidative stress;
apoptosis;
p38 mitogen-activated protein kinase （p38 MAPK）;
Chinese medicine;
mechanism;
research progress
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(9):99-108
- CountryChina
- Language:Chinese
-
Abstract:
Diabetic peripheral neuropathy （DPN） is a symptom and/or sign of peripheral nerve dysfunction that occurs in patients with diabetes mellitus when other causes are excluded. DPN， one of the most common complications of diabetes mellitus， can lead to disability， foot ulcers， and amputation at a later stage. Its pathogenesis is closely related to high glucose-induced inflammatory damage， oxidative stress， mitochondrial disorders， and apoptosis in neural tissues. The p38 mitogen-activated protein kinase （p38 MAPK） signaling pathway is a key mechanism mediating the expression of inflammatory factors， oxidative factors， and apoptotic factors of neural tissues in DPN. The inflammatory response， oxidative stress damage， and apoptosis， induced by the activation of p38 MAPK phosphorylation by factors such as high glucose， can cause cell lipid peroxidation， protein modification， and nucleic acid damage， which results in axonal degeneration and demyelination changes. The current treatment of DPN with western medicine has obvious shortcomings such as adverse effects and addictive tendencies. In recent years， the research on traditional Chinese medicine （TCM） in the prevention and treatment of DPN has gradually increased， and the exploration of Chinese medicine intervention in the p38 MAPK pathway transduction to improve DPN has advanced. The present study reviewed the relations of the p38 MAPK pathway with insulin resistance and peripheral neuropathy and summarized the molecular biological mechanisms involved in the pathological process of DPN， such as inflammation regulation， oxidative stress， polyol pathway regulation， and Schwann cell apoptosis in the past 10 years. In addition， the literature on Chinese medicine monomers， Chinese patent medicines， and Chinese medicine compounds in inhibiting inflammatory reactions， oxidative injury， and apoptosis of DPN peripheral nerves based on the p38 MAPK pathway， resisting axonal degeneration and demyelination changes， improving sensory and motor abnormalities， relieving peripheral pain sensitization， and facilitating nerve conduction mechanism to provide references for the development of new drugs for clinical prevention and treatment of DPN.
