Article Publish Status: FREE
Abstract Title:

AMPK activation by Tanshinone IIA protects neuronal cells from oxygen-glucose deprivation.

Abstract Source:

Oncotarget. 2018 Jan 12 ;9(4):4511-4521. Epub 2017 Dec 17. PMID: 29435120

Abstract Author(s):

Yingfeng Weng, Jixian Lin, Hui Liu, Hui Wu, Zhimin Yan, Jing Zhao

Article Affiliation:

Yingfeng Weng


The current study tested the potential neuroprotective function of Tanshinone IIA (ThIIA) in neuronal cells with oxygen-glucose deprivation (ODG) and re-oxygenation (OGDR). In SH-SY5Y neuronal cells and primary murine cortical neurons, ThIIA pre-treatment attenuated OGDR-induced viability reduction and apoptosis. Further, OGDR-induced mitochondrial depolarization, reactive oxygen species production, lipid peroxidation and DNA damages in neuronal cells were significantly attenuated by ThIIA. ThIIA activated AMP-activated protein kinase (AMPK) signaling, which was essential for neuroprotection against OGDR. AMPKα1 knockdown or complete knockout in SH-SY5Y cells abolished ThIIA-induced AMPK activation and neuroprotection against OGDR. Further studies found that ThIIA up-regulated microRNA-135b to downregulate the AMPK phosphatase Ppm1e. Notably, knockdown of Ppm1e by targeted shRNA or forced microRNA-135bexpression also activated AMPK and protected SH-SY5Y cells from OGDR. Together, AMPK activation by ThIIA protects neuronal cells from OGDR. microRNA-135b-mediated silence of Ppm1e could be the key mechanism of AMPK activation by ThIIA.

Study Type : In Vitro Study

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