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MiR-29 inhibits neuronal apoptosis in rats with cerebral infarction through regulating Akt signaling pathway.

Abstract：

OBJECTIVE:The aim of this study was to explore the influence of micro ribonucleic acid (miR)-29 on neuronal apoptosis in rats with cerebral infarction by regulating the protein kinase B (Akt) signaling pathway. MATERIALS AND METHODS:A total of 36 Sprague-Dawley rats were randomly divided into three groups, including: Sham group (n=12), Model group (n=12), and Inhibitor group (n=12). Common carotid artery, external carotid artery, and internal carotid artery were only exposed in the Sham group. However, the ischemia-reperfusion model was established by the suture method in the other two groups. After modeling, artificial cerebrospinal fluid was injected into the lateral ventricle in the rats of the Sham and Model groups. Similarly, miR-29 inhibitor was injected into the lateral ventricle in the rats of the Inhibitor group. At 24 h postoperatively, the sampling was performed. Zea-Longa score was used to evaluate the neurological deficit of rats. Meanwhile, the expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) in cerebral tissues were detected via immunohistochemistry. The protein expression levels of Akt and phosphorylated Akt (p-Akt) were determined using Western blotting. Furthermore, the expression of miR-29 and cell apoptosis were detected via quantitative Polymerase Chain Reaction (qPCR) and terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) assay, respectively. RESULTS:Compared with Sham group, Model, and Inhibitor groups had substantially raised the Zea-Longa scores (p<0.05). The Zea-Longa score in the Model group was markedly lower than that of the Inhibitor group (p<0.05). The positive expression level of Bax was remarkably upregulated (p<0.05). However, the positive expression level of Bcl-2 declined dramatically in both Model group and Inhibitor group when compared with the Sham group (p<0.05). Besides, the Model group exhibited significantly lower positive expression level of Bax and higher positive expression level of Bcl-2 than the Inhibitor group (p<0.05). The relative protein expression level of p-Akt markedly increased in the Model and Inhibitor groups when compared with the Sham group (p<0.05). However, it was considerably higher in the Model group than that of the Inhibitor group (p<0.05). In comparison with the Sham group, both Model group and Inhibitor group exerted substantially elevated expression level of miR-29 (p<0.05). The relative expression level of miR-29 in the Model group was significantly upregulated when compared with the Inhibitor group (p<0.05). The apoptosis rate of cells in both Model group and Inhibitor group was markedly higher than that of the Sham group (p<0.05). Furthermore, the Model group showed remarkably lower apoptosis rate than the Inhibitor group (p<0.05). CONCLUSIONS:MiR-29 inhibits neuronal apoptosis in cerebral infarction rats by upregulating the Akt signaling pathway, thereby serving as a protector.

journal_name

Eur Rev Med Pharmacol Sci

journal_title

European review for medical and pharmacological sciences

authors

Rong W,Yang L,Li CY,Wu XT,Zhou ZD,Zhu WL,Yan Y

doi

10.26355/eurrev_202001_20068

subject

Has Abstract

pub_date

2020-01-01 00:00:00

pages

843-850

issue

eissn

1128-3602

issn

2284-0729

journal_volume

pub_type

杂志文章

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MiR-29 inhibits neuronal apoptosis in rats with cerebral infarction through regulating Akt signaling pathway.