Wang Manying, Chen Xuenan, Yan Xiuci, Cai Changjiu, Ren Limei, Zhang Shuai, Liu Fangbing
Research Center of Traditional Chinese Medicine, Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China.
Department of Clinical Laboratory, Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, China.
Heliyon. 2024 Jul 30;10(15):e35423. doi: 10.1016/j.heliyon.2024.e35423. eCollection 2024 Aug 15.
In prior reports, Jie-Du-Tong-Luo (JDTL) was reported to help control insulin secretion and blood glucose in patients with diabetes, while also protecting liver and pancreatic islet cells against injury caused by exposure to high glucose (HG) levels. This study was thus developed to assess the effects of JDTL on HG and palmitic acid (PA)-induced muscle injury and to explore the mechanistic basis for these effects.
A model of muscle injury was established using mouse C2C12 myotubes treated with HG + PA. A proteomics approach was used to assess changes in protein levels following JDTL treatment, after which Western immunoblotting was employed to validate significantly affected pathways.
JDTL was able to protect against HG + PA-induced muscle cell injury in this experimental system, altering lipid metabolism and inflammatory activity in these injured C2C12 myotubes. Western blotting suggested that JDTL is capable of activating PI3K/Akt/PPARγ signaling to control lipid metabolism without any corresponding impact on the inflammatory NF-κB pathway.
These data highlight the ability of JDTL to protect against HG + PA-induced injury to muscle cells, and suggest that the underlying basis for such efficacy is related to the PI3K/Akt/PPARγ pathway-mediated modulation of lipid metabolism.
在先前的报告中，据报道解毒通络（JDTL）有助于控制糖尿病患者的胰岛素分泌和血糖，同时还能保护肝脏和胰岛细胞免受高糖（HG）水平暴露所致的损伤。因此，本研究旨在评估JDTL对HG和棕榈酸（PA）诱导的肌肉损伤的影响，并探索这些影响的机制基础。
使用经HG + PA处理的小鼠C2C12肌管建立肌肉损伤模型。采用蛋白质组学方法评估JDTL处理后蛋白质水平的变化，之后使用蛋白质免疫印迹法验证受显著影响的信号通路。
在该实验系统中，JDTL能够保护肌肉细胞免受HG + PA诱导的损伤，改变这些受损C2C12肌管中的脂质代谢和炎症活性。蛋白质免疫印迹法表明，JDTL能够激活PI3K/Akt/PPARγ信号通路以控制脂质代谢，而对炎症性NF-κB信号通路没有相应影响。
这些数据突出了JDTL保护肌肉细胞免受HG + PA诱导损伤的能力，并表明这种功效的潜在基础与PI3K/Akt/PPARγ信号通路介导的脂质代谢调节有关。
