Xinjiang Medical University, Urumqi, 830011, Xinjiang, China.
Traditional Chinese Medicine Hospital Affiliated With Xinjiang Medical University, Urumqi, 830000, Xinjiang, China.
Mol Med. 2023 Jul 18;29(1):98. doi: 10.1186/s10020-023-00698-3.
Diabetic 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.
Rats 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.
CQYG 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.
CQYG exerts neuroprotective effects in experimental diabetic neuropathy through anti-ER stress and anti-apoptosis.
糖尿病周围神经病变（DPN）是糖尿病的主要并发症。本研究旨在探讨复方芪营颗粒（CQYG）治疗 DPN 的疗效及分子机制。
建立 DPN 大鼠和 RSC96 细胞模型，评价 CQYG 的治疗作用。然后检测坐骨神经的形态和凋亡变化。进一步采用串联质量标签定量蛋白质组学技术鉴定差异表达蛋白（DEPs）及其潜在的分子机制。还检测了关键信号通路的蛋白表达。
CQYG 治疗可显著改善血糖和氧化应激水平，并进一步减轻 DPN 大鼠的神经纤维髓鞘病变、去神经和凋亡。进一步发现 CQYG 治疗的 DPN 大鼠有 2176 个 DEPs。富集分析显示，CQYG 治疗后内质网（ER）中的蛋白质加工和细胞凋亡均受到抑制。接下来，CQYG 治疗降低了高糖诱导的 RSC96 细胞中炎症因子表达、线粒体损伤和细胞凋亡。透射电镜结果发现，CQYG 治疗改善了神经髓鞘、线粒体和 ER 的形态。CQYG 治疗降低了 DPN 模型中高表达的 ER 应激和细胞凋亡途径蛋白。此外，我们还预测了 CQYG 在 DEPs 中的潜在靶点。
CQYG 通过抗 ER 应激和抗细胞凋亡对实验性糖尿病神经病变发挥神经保护作用。
