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ARTICLE

Ginsenoside Rg1 protects against ischemia-induced neuron damage by regulating the rno-miRNA-27a-3p/PPARγ axis

YUE GUAN^1,#, TINGTING ZHANG^2,#, JIANAN YU³, JIAWEI LIU⁴, WENYUAN LI⁵, YUJIA ZHENG⁶, JIALE WANG³, YUE LIU³, FENGGUO ZHAI^2,7,*

1 Department of Clinical Medicine, Heilongjiang Nursing College, Harbin, 150001, China
2 Department of Neurology, Hongqi Hospital of Mudanjiang Medical University, Mudanjiang, 157011, China
3 Department of Pharmacology, Mudanjiang Medical University, Mudanjiang, 157011, China
4 Department of Organic Chemistry, Mudanjiang Medical University, Mudanjiang, 157011, China
5 Department of Anatomy, Mudanjiang Medical University, Mudanjiang, 157011, China
6 Department of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Kobe, 654-0142, Japan
7 Institute of Natural Medicine, Mudanjiang Medical University, Mudanjiang, 157011, China

* Corresponding Author: FENGGUO ZHAI. Email:

(This article belongs to the Special Issue: Physiology and Molecular Biology of Plant Stress Tolerance)

BIOCELL 2023, 47(7), 1583-1594. https://doi.org/10.32604/biocell.2023.028016

Received 26 November 2022; Accepted 20 March 2023; Issue published 21 June 2023

Abstract

Background: A preliminary miRNA screening showed that expression levels of rno-miRNA-27a-3p were significantly increased in the serum and brain tissues of rats undergoing cerebral ischemia. In recent years, there is evidence of the protective capacity of the saponins extracted from panax ginseng and its primary active ingredient ginsenosideRg1oncerebral ischemic injury. Methods: Fetal rat neurons (FRNs) were cultured in glucose-and-serum-free medium and exposed to hypoxia to establish a cerebral ischemia model in vitro (oxygen and glucose deprivation model, OGD). Antioxidant indexes (CAT, SOD), inflammatory markers (MPO, TNF-α and IL-6), and the expression of apoptosis and proliferation associated proteins (NF kB-p65, Caspase 3-cleaved, BCL-2) were examined. Results: Pre-treatment of Rg1 (30–100 μg/mL) could effectively inhibit the decline of antioxidant indexes (CAT, SOD) and increase in inflammatory markers (MPO, TNF-α and IL-6), and effectively inhibited the apoptosis in FRNs induced by OGD in a gradient-dependent manner. The mechanism analysis showed that the role of Rg1 in protecting against ischemia-induced neuron damage depends on its indirect up-regulation of PPAR protein via suppression of rno-miRNA-27a-3p. Moreover, these effects of Rg1 could be reversed by exogenous rno-miRNA-27a-3p and PPAR gene silencing in FRNs exposed to OGD. Conclusion: To summarize, our study demonstrates that Rg1 could effectively attenuate neuronal damage caused by cerebral ischemia via the rno-miRNA-27a-3p/PPARγ pathway. Further, clarification of the novel mechanism will certainly improve our previous understanding of the role of Rg1 and enhancing its level in treatments for alleviating ischemic brain injury.

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