Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Serum from rats with electroacupuncture activates the PI3K/Akt signaling pathway to improve synaptic plasticity in HT22 neurons with oxygen and glucose deprivation].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shi Xueke, Chen Tingyu, Gao Jing, Wu Mingli, Li Ruiqing, Su Kaiqi, Lü Zhuan, Song Xiaolei, Feng Xiaodong
Аннотация
OBJECTIVES: To investigate the protective effects of sera from rats receiving electroacupuncture (EA) against oxygen and glucose deprivation/reoxygenation (OGD/R) injury in HT22 neurons and explore the involvement of the PI3K/Akt signaling pathway in this protective mechanism.
METHODS: Bioinformatics analysis was performed using public databases to identify stroke-related pathways. A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were treated with EA at "Shenting" and "Baihui" to prepare EA rat serum. HT22 neurons were subjected to OGD/R and treated with MCAO rat serum, EA rat serum, LY294002, or EA rat serum combined with LY294002. The changes in cell viability, apoptosis, and neuronal morphology were assessed using CCK-8 assay, TUNEL staining, and Nissl staining. Western blotting was used to detect PI3K/Akt phosphorylation and the expressions of the downstream proteins (p-mTOR/mTOR and Bcl-2) and synaptic proteins (NMDAR1 and PSD-95); the mRNA expressions of PI3K, Akt, NMDAR1, and PSD-95 were detected using RT-qPCR.
RESULTS: HT22 neurons with OGD/R injury treated with MCAO rat serum showed significantly decreased cell viability, increased apoptosis, and impaired neuronal morphology, which were obviously improved following treatment with EA rat serum but aggravated after LY294002 treatment. The protective effect of EA rat serum was significantly attenuated by application of LY294002. HT22 neurons treated with MCAO rat serum showed decreased p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR ratios with lowered expressions of Bcl-2, NMDAR1 and PSD-95, which were obviously upregulated by EA rat serum treatment but reduced after LY294002 treatment. The cells with the combined treatment showed intermediate expression levels of these molecules at both the mRNA and protein levels.
CONCLUSIONS: Serum from rats receiving EA at "Shenting" and "Baihui" shows a protective effect against OGD/R injury in HT22 neurons, mediated possibly by activation of the PI3K/Akt signaling pathway and its downstream effectors and upregulation of synaptic plasticity-related molecules.
METHODS: Bioinformatics analysis was performed using public databases to identify stroke-related pathways. A rat model of middle cerebral artery occlusion/reperfusion (MCAO/R) were treated with EA at "Shenting" and "Baihui" to prepare EA rat serum. HT22 neurons were subjected to OGD/R and treated with MCAO rat serum, EA rat serum, LY294002, or EA rat serum combined with LY294002. The changes in cell viability, apoptosis, and neuronal morphology were assessed using CCK-8 assay, TUNEL staining, and Nissl staining. Western blotting was used to detect PI3K/Akt phosphorylation and the expressions of the downstream proteins (p-mTOR/mTOR and Bcl-2) and synaptic proteins (NMDAR1 and PSD-95); the mRNA expressions of PI3K, Akt, NMDAR1, and PSD-95 were detected using RT-qPCR.
RESULTS: HT22 neurons with OGD/R injury treated with MCAO rat serum showed significantly decreased cell viability, increased apoptosis, and impaired neuronal morphology, which were obviously improved following treatment with EA rat serum but aggravated after LY294002 treatment. The protective effect of EA rat serum was significantly attenuated by application of LY294002. HT22 neurons treated with MCAO rat serum showed decreased p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR ratios with lowered expressions of Bcl-2, NMDAR1 and PSD-95, which were obviously upregulated by EA rat serum treatment but reduced after LY294002 treatment. The cells with the combined treatment showed intermediate expression levels of these molecules at both the mRNA and protein levels.
CONCLUSIONS: Serum from rats receiving EA at "Shenting" and "Baihui" shows a protective effect against OGD/R injury in HT22 neurons, mediated possibly by activation of the PI3K/Akt signaling pathway and its downstream effectors and upregulation of synaptic plasticity-related molecules.