Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Ginsenoside Rg1 improves ischemic brain injury by balancing mitochondrial biogenesis and mitophagy

Xuhui Tang , Ningnan Chen, Xiangling Long

Department of Emergency, People's Hospital of Jiangxi Province, Nanchang, Jiangxi, 330006, China;

For correspondence:- Xuhui Tang Email: xuhtang@163.com

Accepted: 28 September 2017 Published: 31 October 2017

Citation: Tang X, Chen N, Long X. Ginsenoside Rg1 improves ischemic brain injury by balancing mitochondrial biogenesis and mitophagy. Trop J Pharm Res 2017; 16(10):2469-2475 doi: 10.4314/tjpr.v16i10.22

© 2017 The authors.
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Abstract

Purpose: To study the effects of ginsenoside Rg1 on mitochondrial dysfunction induced by ischemic stroke.

Methods: Human neuroblastoma SK-N-SH cells, subjected to oxygen-glucose deprivation (OGD), were divided into six groups: control group, OGD group, 3 OGD + Rg1 groups (6.25, 12.5 and 25 μM), and Rg1 (25 μM) group. Apoptosis rate, intracellular production of reactive oxygen species (ROS), and mitochondrial transmembrane potential (MTP) in the OGD cells treated with different concentrations of Rg1 were determined. The mRNA and protein expression levels of mitochondrial biogenesis-related transcription factors and autophagy-related proteins were determined by reat time-polymerase chain reaction (RT-PCR) and Western blotting.

Results: ROS production was significantly increased in OGD SK-N-SH cells (p < 0.01), but this was reversed by Rg1 treatment (p < 0.05). Rg1-treated cells had significantly higher MTP when compared with OGD cells (p < 0.01). Rg1 treatment led to significant increases in mRNA and protein expression levels of PGC1-α, NRF-1, and TFAM-1 (p < 0.01). Moreover, Rg1 treatment inhibited apoptosis in SK-N-SH cells, and up-regulated autophagy-related proteins in t neuronal injury model. Treatment with autophagy inhibitors decreased the mitochondrial protective effects exerted by Rg1 in OGD SK-N-SH cells.

Conclusion: Rg1 improves mitochondrial dysfunction by regulating autophagy in mitochondria. Thus, it may offer protection from brain injuries caused by cerebral ischemia

Keywords: Cerebral ischemia, Ginsenoside Rg1, Mitochondrial dysfunction, Mitophagy