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

作　　者：YUE GUAN TINGTING ZHANG JIANAN YU JIAWEI LIU WENYUAN LI YUJIA ZHENG JIALE WANG YUE LIU FENGGUO ZHAI 

机构地区：[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

出　　处：《BIOCELL》2023年第7期1583-1594,共12页生物细胞（英文）

基　　金：supported by the National Natural Science Foundation of China,Nos.81973317,81374007,81870977;the Natural Science Foundation of Heilongjiang Province,HL2019H062;the Projects of Basic Scientific Research Business Expenses in Higher Education Institutions of Heilongjiang Province,No.2018-KYYWF-MY-005;the Students Innovative and the Entrepreneurship Training Scientific Research Foundation of Heilongjiang Province,No.102292017001.

摘　　要：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-serumfree 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-αand 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(30–100μg/mL)could effectively inhibit the decline of antioxidant indexes(CAT,SOD)and increase in inflammatory markers(MPO,TNF-αand 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 rnomiRNA-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/PPARγpathway.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.

关 键 词：Ginsenoside Rg1 rno-miRNA-27a-3p PPARΓ Cerebral ischemia NEURON OGD 

分 类 号：R741[医药卫生—神经病学与精神病学]