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
By: Zhang, Jidong
.
Contributor(s): Rong, Zhao.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2021Edition: Vol.83(6), Nov-Dec.Description: 1295-1303p.Subject(s): PHARMACEUTICSOnline resources: Click here
In:
Indian journal of pharmaceutical sciencesSummary: 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.
| Item type | Current location | Call number | Status | Date due | Barcode | Item holds |
|---|---|---|---|---|---|---|
Articles Abstract Database
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School of Pharmacy Archieval Section | Not for loan | 2022-1254 |
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.
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