Electroacupuncture reduces corpus callosum injury in rats with permanent cerebral ischemia by inhibiting the activation of high-mobility group box 1 protein and the receptor for advanced glycation end products.

Previous studies have shown that cerebral ischemia can cause white matter injury in the brain. This study aimed to investigate the potential mechanism of electroacupuncture (EA) at the Baihui (GV20) and Zusanli (ST36) acupoints in protecting white matter. Sprague-Dawley rats were used to establish permanent middle cerebral artery occlusion (pMCAO) rat models.

Astragalus Polysaccharide Promotes Neuronal Injury Repair via the Notch1/NFκB Signaling Axis in the Ventroposterior Thalamic Nucleus in Rats with Focal Cerebral Ischemia.

Background: Ischemic stroke is the most common form of stroke and the second most common cause of death and incapacity worldwide. Its pathogenesis and treatment have been the focus of considerable research. In traditional Chinese medicine, the root of Mongolian astragalus has been important in the treatment of stroke since ancient times.

Electroacupuncture protects against the striatum of ischemia stroke by inhibiting the HMGB1/RAGE/p-JNK signaling pathways.

The striatum (Str) is injured 20 min after permanent ischemic stroke, leading to neurological deficits. Here, we aimed to explore the effect of electroacupuncture (EA) on ischemic stroke and elucidate the possible underlying mechanism. Rat permanent middle cerebral artery occlusion (pMCAO) model, EA treatment, sham-EA (SEA) treatment, beam-balance test, hematoxylin and eosin (HE) staining, Nissl staining, immunofluorescence staining, and Western blot were used to investigate the role of EA in pMCAO.

Electroacupuncture reduces cerebral ischemia-induced neuronal damage in the hippocampal CA1 region in rats by inhibiting HMGB1 and p-JNK overexpression.

Background: The cornu ammonis 1 (CA1) region of the hippocampus is a sensitive area that is susceptible to injury caused by cerebral ischemia. High-mobility group box 1 (HMGB1) and phosphorylated c-Jun N-terminal kinase (p-JNK) play important roles in mediating cerebral ischemic injury.

Objective: To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons.

Electroacupuncture inhibits the expression of HMGB1/RAGE and alleviates injury to the primary motor cortex in rats with cerebral ischemia.

Background: The high-mobility group box 1 (HMGB1)/receptor for advanced glycation end products (RAGE) signaling pathway holds promise as a potential therapeutic target for ischemic brain injury. The effects of FPS-ZM1 and electroacupuncture (EA) on activation of the HMGB1/RAGE signaling pathway after cerebral ischemia remain uncertain.

Methods: Middle cerebral artery occlusion (MCAO) model was established.

Regulatory Effect of Electroacupuncture on Hypothalamic Serotonin and its Receptor in Rats with Cerebral Ischemia.

Background: Previous studies have shown that the neurological damage caused by middle cerebral artery occlusion (MCAO) is not only limited to local infarction but can also cause secondary damage in distant sites, such as the hypothalamus. 5-hydroxytryptamine (5-HT)/ 5-HT transporter (5-HTT) and 5-HT receptor 2A (5-HT2A) are important in the treatment of cerebrovascular diseases.

Objective: This study aimed to study the effect of electroacupuncture (EA) on the expression of 5- HT, 5-HTT, and 5-HT2A in the hypothalamus of rats with ischemic brain injury and to explore the protective effect and potential mechanism of EA on the secondary injury of cerebral ischemia.