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异黄酮通过激活雌激素受体-PI3K-Akt信号通路协同减轻脑缺血再灌注损伤。

Isoflavones Synergistically Alleviate Cerebral Ischemia and Reperfusion Injury Activating Estrogen Receptor-PI3K-Akt Signaling Pathway.

作者信息

Gu Yong, Chen Xi, Fu Shuping, Liu Wenlan, Wang Qi, Liu Ke-Jian, Shen Jiangang

机构信息

Clinical Research Center, Hainan Provincial Hospital of Chinese Medicine, Haikou, China.

School of Chinese Medicine, University of Hong Kong, Hong Kong, China.

出版信息

Front Pharmacol. 2021 Feb 22;12:533028. doi: 10.3389/fphar.2021.533028. eCollection 2021.

DOI:10.3389/fphar.2021.533028
PMID:33692686
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7937971/
Abstract

Isoflavones are major neuroprotective components of a medicinal herb against cerebral ischemia-reperfusion injury but the mechanisms of neuroprotection remain unclear. Calycosin and formononetin are two major AR isoflavones while daidzein is the metabolite of formononetin after absorption. Herein, we aim to investigate the synergistic neuroprotective effects of those isoflavones of against cerebral ischemia-reperfusion injury. Calycosin, formononetin and daidzein were organized with different combinations whose effects observed in both and experimental models. In the study, primary cultured neurons were subjected to oxygen-glucose deprivation plus reoxygenation (OGD/RO) or l-glutamate treatment. In the study, rats were subjected to middle cerebral artery occlusion to induce cerebral ischemia and reperfusion. All three isoflavones pre-treatment alone decreased brain infarct volume and improved neurological deficits in rats, and dose-dependently attenuated neural death induced by l-glutamate treatment and OGD/RO in cultured neurons. Interestingly, the combined formulas of those isoflavones revealed synergistically activated estrogen receptor (estrogen receptors)-PI3K-Akt signaling pathway. Using ER antagonist and phosphatidylinositol 3-kinase (PI3K) inhibitor blocked the neuroprotective effects of those isoflavones. In conclusion, isoflavones could synergistically alleviate cerebral ischemia-reperfusion injury activating ER-PI3K-Akt pathway.

摘要

异黄酮是一种药草中对抗脑缺血再灌注损伤的主要神经保护成分，但神经保护机制仍不清楚。毛蕊异黄酮和芒柄花素是两种主要的芳基异黄酮，而大豆苷元是芒柄花素吸收后的代谢产物。在此，我们旨在研究这些异黄酮对脑缺血再灌注损伤的协同神经保护作用。将毛蕊异黄酮、芒柄花素和大豆苷元以不同组合进行配制，并在细胞和动物实验模型中观察其效果。在细胞实验中，原代培养的神经元接受氧葡萄糖剥夺加复氧（OGD/RO）或L-谷氨酸处理。在动物实验中，大鼠接受大脑中动脉闭塞以诱导脑缺血和再灌注。单独使用这三种异黄酮预处理均可减少大鼠脑梗死体积并改善神经功能缺损，且剂量依赖性地减轻L-谷氨酸处理和OGD/RO诱导的培养神经元中的神经死亡。有趣的是，这些异黄酮的联合配方显示出协同激活雌激素受体（ER）-PI3K-Akt信号通路。使用ER拮抗剂和磷脂酰肌醇3激酶（PI3K）抑制剂可阻断这些异黄酮的神经保护作用。总之，异黄酮可通过激活ER-PI3K-Akt通路协同减轻脑缺血再灌注损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d11b0a64bebf/fphar-12-533028-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/c797a23d0bf2/fphar-12-533028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d371abec933b/fphar-12-533028-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/81ad64916c94/fphar-12-533028-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/6b59e148daa2/fphar-12-533028-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d1d9807a354c/fphar-12-533028-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d11b0a64bebf/fphar-12-533028-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/c797a23d0bf2/fphar-12-533028-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d371abec933b/fphar-12-533028-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/81ad64916c94/fphar-12-533028-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/6b59e148daa2/fphar-12-533028-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d1d9807a354c/fphar-12-533028-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb30/7937971/d11b0a64bebf/fphar-12-533028-g006.jpg

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