Article Publish Status: FREE
Abstract Title:

Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3Pathway in Neuroblastoma SH-SY5Y Cells.

Abstract Source:

Biomed Res Int. 2020 ;2020:1562915. Epub 2020 Aug 6. PMID: 32832542

Abstract Author(s):

Rui Li, Wenzhou Liu, Li Ou, Feng Gao, Min Li, Liping Wang, Peifeng Wei, Feng Miao

Article Affiliation:

Rui Li


Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting HO-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated HO-induced inflammatory factors, including IL-6, NO, and TNF-, and alleviated HO-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3signaling pathway. What is more, the PI3K/mTOR/GSK3pathway participated in the protective mechanism of emodin on HO-induced cell damage. Collectively, it suggests that emodin alleviates HO-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3signaling pathway.

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