2. Academic Validation
  3. Protective Effects and Mechanisms of MicroRNA-182 on Oxidative Stress in RHiN

Protective Effects and Mechanisms of MicroRNA-182 on Oxidative Stress in RHiN

  • Open Life Sci. 2019 Aug 28:14:400-409. doi: 10.1515/biol-2019-0045.
Lihua Li 1,  Wenna Peng 2,  Xiangrong Tian 3
Affiliations

Affiliations

  • 1 Colleges of Medicine, Jishou University, Jishou, Hunan Province, P.R. China.
  • 2 Department of Rehabilitation Medicine, The Second Xiangya Hospital of Central South University, Changsha, Hunan Province, P.R. China.
  • 3 Biology and Environmental Sciences, Jishou University, Jishou, Hunan Province, P.R. China.
PMID: 33817175 DOI: 10.1515/biol-2019-0045
Abstract

To explore protective effects and related mechanisms of microRNA-182 (miR-182) on oxidative stress in rat hippocampal neurons (RHiN), RHiN cells. As the results, the survival rate and superoxide dismutase levels in H2O2 group were significantly lower than H2O2+miR-182 group (all P<0.05). The malondialdehyde levels and Apoptosis rate in H2O2+miR-182 group were significantly lower than H2O2 group (all P<0.05). The mRNA levels and expression levels of mTOR and PI3K in H2O2+miR-182 group were higher than those in H2O2 group (both P<0.05). The experiment of cerebral ischemic oxidative stress model rats showed that the survival rate, Apoptosis rate, malondialdehyde and superoxide dismutase levels in miR-182 group were better than model control group. The positive staining intensity of phosphoinositide 3-kinase (mTOR) and phosphoinositide 3-kinase (PI3K) in model control group were significantly lower than miR-182 group (all P<0.05). Increased levels of miR-182 can reduce the damage of H2O2 treatments in RHiN cells. Oxidative stress is decreased in the neuronal cells possibly by activation of the PI3K-AKT-mTOR pathway.

Keywords

miR-182; oxidative stress; rat hippocampal neurons.

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