Zhang, Jidong
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 - Vol.83(6), Nov-Dec - Mumbai Indian Journal of Pharmaceutical Science 2021 - 1295-1303p.
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-expression, 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.
PHARMACEUTICS
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 - Vol.83(6), Nov-Dec - Mumbai Indian Journal of Pharmaceutical Science 2021 - 1295-1303p.
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-expression, 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.
PHARMACEUTICS