The International journal of neuroscience · 2023
Electroacupuncture reduces cerebral ischemia-induced neuronal damage in the hippocampal CA1 region in rats by inhibiting HMGB1 and p-JNK overexpression.
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Zhao Jian, Nie Zeyin, Miao Huachun, Wu Feng, Ma Tongjun
Аннотация
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.
METHODS: A rat model of permanent middle cerebral artery occlusion (pMCAO) was established. Sprague-Dawley rats were divided into four groups: sham-operated control, pMCAO control, EA, and sham-EA (SEA). In the EA and SEA groups, the GV20 and ST36 acupoints were selected for treatment. However, the SEA group was treated only by superficial pricking of the skin at the two acupoints without the application of electricity. Neurological function was assessed using the neurological deficit function score, and neuronal damage was detected through Nissl staining. HMGB1 and p-JNK expression was evaluated using immunohistochemical staining and western blot assays.
RESULTS: The behavioural experiments showed that the EA treatment improved the neurological deficits in the pMCAO rats. The Nissl staining results revealed that EA reduced neural tissue damage. The immunohistochemical staining and western blot results showed that EA inhibited HMGB1 and p-JNK overexpression. By contrast, none of these EA effects were observed in the SEA group.
CONCLUSION: EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.
OBJECTIVE: To elucidate the mechanism through which electroacupuncture (EA) via the Baihui (GV20) and Zusanli (ST36) acupoints protects neurons.
METHODS: A rat model of permanent middle cerebral artery occlusion (pMCAO) was established. Sprague-Dawley rats were divided into four groups: sham-operated control, pMCAO control, EA, and sham-EA (SEA). In the EA and SEA groups, the GV20 and ST36 acupoints were selected for treatment. However, the SEA group was treated only by superficial pricking of the skin at the two acupoints without the application of electricity. Neurological function was assessed using the neurological deficit function score, and neuronal damage was detected through Nissl staining. HMGB1 and p-JNK expression was evaluated using immunohistochemical staining and western blot assays.
RESULTS: The behavioural experiments showed that the EA treatment improved the neurological deficits in the pMCAO rats. The Nissl staining results revealed that EA reduced neural tissue damage. The immunohistochemical staining and western blot results showed that EA inhibited HMGB1 and p-JNK overexpression. By contrast, none of these EA effects were observed in the SEA group.
CONCLUSION: EA may reduce ischemia-induced neuronal damage in the hippocampal CA1 region by inhibiting the overexpression of both HMGB1 and p-JNK.