Electroacupuncture Alleviates Ischemic Stroke by Activating the mTOR/SREBP1 Pathway

Objective: Ischemic stroke (IS) is one of the leading causes of death and disability worldwide. Electroacupuncture (EA) has been shown to exert a neuroprotective effect in IS. However, the specific anti-IS mechanisms of EA remain to be further elucidated. Thus, we aimed to investigate the anti-IS role of EA and its mechanism. Methods: By constructing a rat IS (middle cerebral artery occlusion, MCAO) model and performing EA treatment, the neurological deficit score, brain water content, and cerebral infarction were evaluated. ELISA was used to measure the levels of oxidative stress (OS)-related molecules (MDA, SOD, GSH, and CAT). Ferroptosis-related proteins (GPX4, SLC7A11, TfR1, L-ferritin, and hepcidin), neurological damage-related proteins (GFAP, Iba-1, and Nestin), α7nAChR, and mTOR pathway-related proteins (mTOR, p-mTOR, and SREBP1) in rat brain penumbra were assessed using western blotting. Results: Following EA treatment, the neurological deficit score, brain water content, cerebral infarction, and GFAP, Iba-1, and Nestin expression were reduced in the brain penumbra of MCAO rats. Additionally, EA treatment decreased MDA level and increased SOD, GSH, and CAT levels in the brain penumbra of MCAO rats. Moreover, MCAO rats showed elevated GPX4 and SLC7A11 expression and reduced TfR1, L-ferritin, and hepcidin in the brain penumbra following EA treatment. After EA treatment, α7nAChR, mTOR, p-mTOR, and SREBP1 expression were upregulated in the brain penumbra of MCAO rats. Conclusions: EA treatment inhibited OS and ferroptosis to exert a neuroprotective effect in IS, which might be realized via the activation of mTOR/SREBP1 signaling.