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

Yingfeng Weng; Jixian Lin; Hui Liu; Hui Wu; Zhimin Yan; Jing zhao

doi:10.18632/oncotarget.23391

Oncotarget

Oncotarget (a primarily oncology-focused, peer-reviewed, open access journal) aims to maximize research impact through insightful peer-review; eliminate borders between specialties by linking different fields of oncology, cancer research and biomedical sciences; and foster application of basic and clinical science.

Its scope is unique. The term "oncotarget" encompasses all molecules, pathways, cellular functions, cell types, and even tissues that can be viewed as targets relevant to cancer as well as other diseases. The term was introduced in the inaugural Editorial, Introducing Oncotarget.

As of January 1, 2022, Oncotarget has shifted to a continuous publishing model. Papers will now be published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Subscribe to receive alerts once a paper has been published by Oncotarget.

Impact Journals, LLC is the publisher of Oncotarget: www.impactjournals.com.

Impact Journals is a member of the Wellcome Trust List of Compliant Publishers.

Impact Journals is a member of the Society for Scholarly Publishing.

On December 23, 2022, Oncotarget server experienced a DDoS attack. As a result, Oncotarget site was inaccessible for a few hours. Oncotarget team swiftly dealt with the situation and took it under control. This malicious action will be reported to the FBI.

Research Papers:

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

Yingfeng Weng, Jixian Lin, Hui Liu, Hui Wu, Zhimin Yan and Jing zhao _

PDF | HTML | How to cite

Oncotarget. 2018; 9:4511-4521. https://doi.org/10.18632/oncotarget.23391

Metrics: PDF 1417 views | HTML 2794 views | ?

Abstract

Yingfeng Weng1,*, Jixian Lin1,*, Hui Liu1,*, Hui Wu1, Zhimin Yan1 and Jing Zhao1

1Department of Neurology, Minhang Branch, Zhongshan Hospital, Fudan University, Shanghai, China

*Co-first authors

Correspondence to:

Jing Zhao, email: [email protected]

Zhimin Yan, email: [email protected]

Keywords: OGDR; neuroprotection; Tanshinone IIA; AMP-activated protein kinase (AMPK); Ppm1e

Received: October 27, 2017 Accepted: December 01, 2017 Published: December 17, 2017

ABSTRACT

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-135b expression 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.

All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 23391

Publication Alerts

Research Papers:

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

Abstract