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 SKN- 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
Highlights
Stroke is the third most deadly disease in the world and a major source of disability [1]
The results showed that reactive oxygen species (ROS) production was significantly increased in SK-N-SH cells subjected to oxygen-glucose deprivation (OGD) (p < 0.01 relative to the control group; Figure 2)
SK-N-SH cells underwent OGD showed a slightly increased pattern of expressions of the mitochondrial biogenesis related transcription factors PGC1-α, NRF-1, and TFAM-1, as determined by reat time-polymerase chain reaction (RT-PCR) (Figure 4B), as well as increases in protein levels detected by Western blotting (Fig. 4A)
Summary
Stroke is the third most deadly disease in the world and a major source of disability [1]. Known as cerebral ischemia, accounts for about 65-80 % of strokes, and is caused by lack of cerebral blood flow due to a variety of factors [1,2]. Cell autophagy is extensively involved in various stages of cerebral ischemia [3]. Autophagy is a self-regulating defensive adaptation process in eukaryotic cells [3,4]. It is expected to provide raw materials for cell repair and reconstruction to meet the normal turnover and cyclic utilization of cytoplasmic components. It has an important regulatory role in maintaining the stability of the intracellular environment, cell growth, and development [3,4]
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