Electroacupuncture attenuated cerebral ischemia injury correlated with increased glucose consumption and elevated...

Cerebral ischemic stroke (IS) is a prevalent cerebrovascular accident that can lead to severe consequences. Electroacupuncture (EA) has demonstrated efficacy in alleviating cerebral ischemia/reperfusion (I/R) injury; however, the underlying molecular mechanisms remain poorly understood. It has been reported that the upregulation of glucose transporter gene expressions restores the ability of cerebral cells to consume energy during I/R. However, whether the use of EA affects glucose metabolism remains elusive. This study tries to elucidate the role of EA in regulating glucose metabolism during cerebral I/R process.

Rats with middle cerebral artery occlusion (MCAO) were employed as cerebral I/R injury models, and EA were performed at Baihui and Shenting acupoints in the modeled rats as treatment strategies. Additionally, Magnetic Resonance Imaging (MRI) was employed to measure cerebral infarction volume, Positron Emission Tomography/Computed Tomography (PET/CT) to evaluate glucose uptake in the hippocampus, neurological deficit scoring along with Morris Water Maze (MWM) testing was used to assess neurological deficits, and Western blot and Enzyme-linked Immunosorbent Assay (ELISA) tests determined the expression levels of glucose transporters genes GLUT1 and GLUT3.

Neurological deficit scoring and MWM test results indicated that EA at Baihui and Shenting acupoints significantly alleviated neurological deficits caused by I/R injury. MRI results also showed that the treatment reduced the cerebral infarction volume. Moreover, PET/CT outcome revealed that EA at the two acupoints enhanced glucose uptake and metabolism in the injured cerebral hippocampus. At the molecular level, EA at the two acupoints significantly upregulated the expression of glucose transporter genes GLUT1 and GLUT3, as evidenced by Western blot results.

EA at Baihui and Shenting acupoints can ameliorate I/R injury and facilitate glucose uptake and metabolism by promoting the expression of hippocampal glucose transporter genes GLUT1 and GLUT3.