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Hydroxysafflor yellow A (HSYA) alleviates apoptosis and autophagy of neural stem cells induced by heat stress via p38 MAPK/MK2/Hsp27-78 signaling pathway.

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机构： [1]Department of Intensive Care Unit, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China [2]Department of Intensive Care Unit, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China [3]Department of Traditional Chinese Medicine Surgery, Jilin People’s Hospital, Jilin, 132000, China [4]Intensive Care Unit, Clifford Hospital, Guangzhou University of Chinese Medicine, No.3 Hongfu Road, Panyu District, Guangzhou 511495, PR China [5]Department of Emergency, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, No. 16 Jichang Road, Baiyun District, Guangzhou, 510405, China

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关键词： Hydroxysafflor yellow A Neural stem cells Apoptosis Autophagy MAPK signaling pathway

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This study aimed to explore mechanisms of the effects of hydroxysafflor yellow A (HSYA) on neural stem cells (NSCs) after heat stress (HS). Rat NSCs cells were cultured at 42 °C to impose heat stress. Cell counting kit-8 and Edu assay were used to analyze NSC proliferation. Annexin V/PI apoptosis kit was used to detect NSC apoptosis. Expression and phosphorylation of autophagy and apoptosis-associated proteins were determined by western blotting. We showed that HSYA significantly promoted proliferation and attenuated apoptosis of NSCs after heat stress. HSYA also increased Bcl-2 expression but decreased the expression of Bax and cleaved caspase-3 in NSCs induced by heat stress. In addition, HSYA decreased p38 and Hsp27-78 phosphorylation and MK-2 expression after heat stress, which was consistent with NSCs treated with SB203850 treatment or p38 knockdown. Furthermore, we demonstrated that heat stress increased LC3-II expression and mTOR phosphorylation, and decreased the expression of p62 in NSCs, while HSYA, SB203850 treatment or p38 knockdown reversed these alterations. In conclusion, HSYA significantly reversed the apoptosis and autophagy of NSCs induced by heat stress (P < 0.05), via downregulating MK2 expression and p38 and Hsp27-78 phosphorylation. Copyright © 2019. Published by Elsevier Masson SAS.

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出版当年[2018]版：

大类 | 3 区医学

小类 | 3 区医学：研究与实验 3 区药学

最新[2025]版：

大类 | 2 区医学

小类 | 2 区医学：研究与实验 2 区药学

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第一作者机构： [1]Department of Intensive Care Unit, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510405, China

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