miR-130a alleviates neuronal apoptosis and changes in expression of Bcl-2/Bax and caspase-3 in cerebral infarction rats through PTEN/PI3K/Akt signaling pathway.

Published on Jan 3, 2020in Experimental and Therapeutic Medicine1.785
· DOI :10.3892/ETM.2020.8415
Yinming Wang1
Estimated H-index: 1
,
Junquan Gu1
Estimated H-index: 1
+ 5 AuthorsShuhua Gui1
Estimated H-index: 1
Sources
Abstract
Effect of micro ribonucleic acid (miR)-130a on neuronal apoptosis in rats with cerebral infarction (CI) was studied to explore whether phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) is involved in the regulation of neuronal apoptosis. Thirty-six Sprague-Dawley (SD) rats were randomly divided into blank control group, model group and miR-130a low-expression group. miR-130a was determined by quantitative polymerase chain reaction (qPCR), the content of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and IL-10 was detected using the enzyme-linked immunosorbent assay (ELISA) kits, and the neuronal apoptosis level in each group was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The neurobehavioral score was significantly lower in model group than that in blank control group (P<0.01), while it was significantly higher in miR-130a low-expression group than that in model group (P<0.01). Compared with blank control group, the model group had obviously increased content of TNF-alpha and IL-6 (P<0.01), decreased content of IL-10 (P<0.01), more apoptotic neurons (P<0.01), higher expression of caspase-3 (P<0.01), and obviously lower Bcl-2/Bax (P<0.01). Moreover, expression of phosphorylated (p)-PTEN, PI3K and p-Akt in brain tissues was remarkably lower in the model group than those in the blank control group (P<0.01). The expression level of miR-130a in brain tissues of CI rats is significantly increased. miR-130a promotes the release of inflammatory factors and facilitates neuronal apoptosis through suppressing the PTEN/PI3K/Akt signaling pathway.
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