Ginsenoside Rg5 Alleviates 1-Methyl-4-Phenylpyridinium Ion Induced Parkinson's Disease Cell Model Damage by Regulating MicroRNA-874-3p/Thioredoxin Interacting Proteins Molecular Axis
Department of Pharmacy, School Hospital, Huazhong University of Science and Technology, Wuhan 430074, 1Surgical Department, School Hospital, Huazhong University of Science and Technology, Wuhan 430074, 2Department of Pharmacy, Liyuan Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430077, China
Xuju Sun, Department of Pharmacy, Liyuan Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430077, China, E-mail: email@example.com
This research attempts to probe into the influence mechanism of ginsenoside Rg5 on 1-methyl-4- phenylpyridine ion induced Parkinson's disease cell model damage. Different concentrations (25, 50, 100 μmol/l) of ginsenoside Rg5 acted on human neuroblastoma SK-N-SH cells induced by 1-methyl-4- phenylpyridine ion. Adopt cell counting kit-8, flow cytometry, quantitative reverse transcription polymerase chain reaction and western blot to exam cell viability, apoptosis rate, microRNA-874-3p and thioredoxin interacting proteins expressions. Transfected microRNA-874-3p mimics and thioredoxin interacting proteins small interfering RNA to SK-N-SH cells, respectively. Then adopt the above mentioned methods to exam microRNA-874-3p overexpression or thioredoxin interacting proteins inhibition influence on SK-N-SH cells viability and apoptosis which is induced by 1-methyl-4-phenylpyridine ion. Adopt dual luciferase report experiment and western blot methods to test the regulatory function of microRNA- 874-3p on thioredoxin interacting proteins. After ginsenoside Rg5 acted on 1-methyl-4-phenylpyridine ion induced SK-N-SH cells, the cell viability and microRNA-874-3p expression increased significantly, but thioredoxin interacting proteins expression and apoptosis rate decreased significantly (p<0.05). After microRNA-874-3p over-expressing, 1-methyl-4-phenylpyridine ion induced SK-N-SH cells viability were significantly increased and apoptosis rate was remarkably reduced (p<0.05). After inhibiting thioredoxin interacting proteins expression, 1-methyl-4-phenylpyridine ion induced SK-N-SH cells viability was significantly increased, but apoptosis rate was remarkably lowered (p<0.05). MicroRNA-874-3p regulates thioredoxin interacting proteins expression negatively. MicroRNA-874-3p inhibition could attenuate the effect of ginsenoside Rg5 on the viability and apoptosis of 1-methyl-4-phenylpyridine ion induced SK-N-SH (p<0.05). Thioredoxin interacting proteins inhibition went into reverse microRNA-874-3p inhibition combined with ginsenoside Rg5 treatment on 1-methyl-4-phenylpyridine ion induced SK-N-SH activity and apoptosis (p<0.05). Ginsenoside Rg5 could alleviate 1-methyl-4-phenylpyridine ion induced Parkinson's disease cell model damage and its mechanism possibly has relationship with the up-regulation of microRNA-874-3p/thioredoxin interacting proteins molecular axis.