Electroacupuncture alleviates motor dysfunction after intracerebral hemorrhage via the PPARγ-EAAT2 pathway.

Nowadays, intracerebral hemorrhage (ICH) is the main cause of death and disability, and motor impairment is a common sequel to ICH. Electroacupuncture (EA) has been widely used for functional recovery after ICH. However, its role and associated regulatory mechanisms in rehabilitation after ICH remain poorly understood. This study investigated whether EA can have a neuroprotective effect in motor function after ICH by inhibiting glutamate-mediated excitotoxicity on the primary motor cortex. The model was established using autologous tail artery blood, followed by administration of EA at Quchi (LI11) and Zusanli (ST36) for 3 or 7 consecutive days. The rats' behavior was examined by modified neurological severity score (mNSS) and open-field test (OFT). Nissl staining, immunofluorescence detection, and transmission electron microscopy were used to observe the degree of neuron damage. The level of the cortical glutamate was detected by the ELISA. Peroxisome proliferator-activated receptor gamma (PPARγ) expression was detected by immunohistochemistry and western blot. The protein and mRNA expression of excitatory amino acid transporter 2 (EAAT2) was detected by western blot and quantitative real-time PCR. Our data demonstrated that EA significantly reduces glutamate levels, alleviates neuronal damage, and promotes motor function recovery in rats after ICH. In addition, EA upregulates PPARγ and EAAT2 expression. However, the protective effect of EA on motor function and EAAT2 expression are partially abolished by T0070907, an antagonist of PPARγ. EA at LI11 and ST36 improved glutamate excitotoxicity and promoted motor function recovery after ICH by activating the PPARγ-EAAT2 pathway and reducing the glutamate level.