Compound Qiying Granules alleviates diabetic peripheral neuropathy by inhibiting endoplasmic reticulum stress and apoptosis

Molecular Medicine

Research Article

Guanying Wang¹  Jinxia Hu²  Xiaoling Hu²  Xiaolin Xie³  Zhiyan Liu³  Zhengting Liang³  Yan Hu³  Chen Chen³  Tao Liu⁴ 

[1] Guizhou University of Traditional Chinese Medicine, 550025, Guiyang, Guizhou, China;Traditional Chinese Medicine Hospital Affiliated With Xinjiang Medical University, 830000, Urumqi, Xinjiang, China;Xinjiang Medical University, 830011, Urumqi, Xinjiang, China;Xinjiang Medical University, 830011, Urumqi, Xinjiang, China;Traditional Chinese Medicine Hospital Affiliated With Xinjiang Medical University, 830000, Urumqi, Xinjiang, China;

关键词: Diabetic peripheral neuropathy;    CQYG;    ER stress;    Apoptosis;    Differentially expressed proteins;   

DOI  :  10.1186/s10020-023-00698-3

 received in 2023-01-07, accepted in 2023-07-11,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundDiabetic peripheral neuropathy (DPN) is a major complication of diabetes. This study aimed to investigate the therapeutic effects and molecular mechanisms of Compound Qiying Granules (CQYG) for DPN.MethodsRats and RSC96 cells of DPN models were established to evaluate the therapeutic effects of CQYG. Then the morphology and apoptotic changes of sciatic nerves were detected. Further, tandem mass tag based quantitative proteomics technology was used to identify differentially expressed proteins (DEPs) and the underlying molecular mechanisms. Protein expression of key signaling pathways was also detected.ResultsCQYG treatment significantly improved blood glucose and oxidative stress levels, and further reduced nerve fiber myelination lesions, denervation, and apoptosis in DPN rats. Further, 2176 DEPs were found in CQYG treated DPN rats. Enrichment analysis showed that protein processing in the endoplasmic reticulum (ER), and apoptosis were all inhibited after CQYG treatment. Next, CQYG treatment reduced inflammatory factor expression, mitochondrial damage, and apoptosis in RSC96 cells which induced by high glucose. Transmission electron microscopy results found that CQYG treatment improved the morphology of nerve myelin, mitochondria, and ER. CQYG treatment decreased ER stress and apoptosis pathway proteins that were highly expressed in DPN models. In addition, we also predicted the potential targets of CQYG in DEPs.ConclusionsCQYG exerts neuroprotective effects in experimental diabetic neuropathy through anti-ER stress and anti-apoptosis.

【 授权许可】

CC BY   
© The Author(s) 2023

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