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乳酸通过激活电压门控钙通道改善棕榈酸酯诱导的C2C12细胞分化能力损伤。

Lactate ameliorates palmitate-induced impairment of differentiative capacity in C2C12 cells through the activation of voltage-gated calcium channels.

作者信息

Wan Juan, Cheng Chunfang, Li Xiaonuo, Zhu Yuanjie, Su Hu, Gong Yanchun, Ding Kaizhi, Gao Xiaofei, Dang Caixia, Li Guoyin, Jiang Wei, Yao Li-Hua

机构信息

School of Sport Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi, 330013, People's Republic of China.

School of Life Science, Jiangxi Science & Technology Normal University, Nanchang, Jiangxi, 330013, People's Republic of China.

出版信息

J Physiol Biochem. 2024 May;80(2):349-362. doi: 10.1007/s13105-024-01009-y. Epub 2024 Feb 19.

DOI:10.1007/s13105-024-01009-y
PMID:38372933
Abstract

Palmitic acid (PA), a saturated fatty acid enriched in high-fat diet, has been implicated in the development of skeletal muscle regeneration dysfunction. This study aimed to examine the effects and mechanisms of lactate (Lac) treatment on PA-induced impairment of C2C12 cell differentiation capacity. Furthermore, the involvement of voltage-gated calcium channels in this context was examined. In this study, Lac could improve the PA-induced impairment of differentiative capacity in C2C12 cells by affecting Myf5, MyoD and MyoG. In addition, Lac increases the inward flow of Ca, and promotes the depolarization of the cell membrane potential, thereby activating voltage-gated calcium channels during C2C12 cell differentiation. The enchancement of Lac on myoblast differentiative capacity was abolished after the addition of efonidipine (voltage-gated calcium channel inhibitors). Therefore, voltage-gated calcium channels play an important role in improving PA-induced skeletal muscle regeneration disorders by exercising blood Lac. Our study showed that Lac could rescue the PA-induced impairment of differentiative capacity in C2C12 cells by affecting Myf5, MyoD and MyoG through the activation of voltage-gated calcium channels.

摘要

棕榈酸(PA)是一种富含于高脂饮食中的饱和脂肪酸,与骨骼肌再生功能障碍的发生有关。本研究旨在探讨乳酸(Lac)处理对PA诱导的C2C12细胞分化能力损伤的影响及机制。此外,还研究了电压门控钙通道在此过程中的作用。在本研究中,Lac可通过影响Myf5、MyoD和MyoG改善PA诱导的C2C12细胞分化能力损伤。此外,Lac增加Ca的内流,促进细胞膜电位去极化,从而在C2C12细胞分化过程中激活电压门控钙通道。加入依福地平(电压门控钙通道抑制剂)后,Lac对成肌细胞分化能力的增强作用被消除。因此,电压门控钙通道通过调节血液中的Lac在改善PA诱导的骨骼肌再生障碍中起重要作用。我们的研究表明,Lac可通过激活电压门控钙通道影响Myf5、MyoD和MyoG,从而挽救PA诱导的C2C12细胞分化能力损伤。

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