TITLE:
Electroacupuncture Improves Rat Traumatic Brain Injury by Affecting Mitochondrial Function through the AMPK-PGC1α/SIRT1 Pathway
AUTHORS:
Bingxue Zhang, Liangmin Gao, Ya Li, Baocai Hong, Xiongli Fu, Pinwen Tu, Chaochao Yang, Yongqian Deng, Yunbin Sun, Yinghong He, Hongbo Chen
KEYWORDS:
Traumatic Brain Injury, Electroacupuncture, Mitochondrial Function, AMPK, PGC-1α, SIRT1
JOURNAL NAME:
American Journal of Molecular Biology,
Vol.16 No.4,
October
10,
2026
ABSTRACT: Background and Purpose: Traumatic brain injury (TBI) is a common clinical craniocerebral injury. Not only does it affect the psychology and physiology of patient health, but it places a serious burden on the family and socioeconomic profile of patients. Although current studies have shown that electroacupuncture (EA) treatment is preliminarily effective for treating TBI, the specific mechanism is still unclear. Therefore, this study aimed to investigate the mechanism of action of EA in TBI. Methods: A rat TBI model was induced by controlled cortical impact (CCI). Rat brain tissue damage was evaluated by measuring the water content of the brain tissue. The assessment of neural function and the damage to learning and memory functions in rats was conducted through the modified neurological severity score (mNSS) and the Morris water maze experiment. ATP content was detected using a kit. Mitochondrial reactive oxygen species (mROS) levels and mitochondrial membrane potential were detected by flow cytometry. The expression of key genes and proteins was detected by RT-qPCR and Western blotting. Results: After TBI, the water content of the brain tissue significantly increased, and the neural, learning, and memory functions of the rats were impaired, which improved after EA treatment. In addition, after TBI, rats showed decreased ATP levels, mitochondrial membrane potential, and p-AMPK/AMPK, PGC-1α, and SIRT1 expression, along with increased mROS levels. EA treatment reversed these effects. Conclusion: Our research indicates that EA can enhance mitochondrial function through the activation of the AMPK-PGC-1α/SIRT1 pathway, thereby improving TBI-induced neurological dysfunction.