Icariin inhibits apoptosis in OGD-induced neurons by regulating M2 pyruvate kinase.

淫羊藿苷通过调节 M2 丙酮酸激酶抑制 OGD 诱导的神经元凋亡

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作者:Chen Shan, Zou Renfang, Si Jiayi, Shi Qianzhi, Zhang Lu, Kang Lina, Ni Jie, Sha Dujuan
BACKGROUND: Ischaemic stroke can lead to many complications, but treatment options are limited. Icariin is a traditional Chinese medicine with reported neuroprotective effects against ischaemic cerebral injury; however, the underlying mechanisms by which icariin ameliorates cell apoptosis require further study. PURPOSE: This study aimed to investigate the therapeutic potential of icariin after ischaemic stroke and the underlying molecular mechanisms. METHODS: N2a neuronal cells were used to create an in vitro oxygen-glucose deprivation (OGD) model. The effects of icariin on OGD cells were assessed using the CCK-8 kit to detect the survival of cells and based on the concentration, apoptosis markers, inflammation markers, and M2 pyruvate kinase isoenzyme (PKM2) expression were detected using western blotting, RT-qPCR, and flow cytometry. To investigate the underlying molecular mechanisms, we used the PKM2 agonist TEPP-46 and detected apoptosis-related proteins. RESULTS: We demonstrated that icariin alleviated OGD-induced apoptosis in vitro. The expression levels of the apoptosis marker proteins caspase-3 and Bax were upregulated and Bcl-2 was downregulated. Furthermore, icariin reduced inflammation and downregulated the expression of PKM2. Moreover, activation of the PKM2 by pretreatment with the PKM2 agonist TEPP-46 enhanced the effects on OGD induced cell apoptosis in vitro. CONCLUSION: This study elucidated the underlying mechanism of PKM2 in OGD-induced cell apoptosis and highlighted the potential of icariin in the treatment of ischaemic stroke.

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