Mechanism of hyperbaric oxygen alleviating cerebral infarction in rats via regulating miR-153-3p/Bcl-2 axis
10.3760/cma.j.cn311847-20200827-00335
- VernacularTitle:高压氧调控miR-153-3p/Bcl-2轴缓解大鼠脑梗死的作用机制
- Author:
Lan ZHANG
1
;
Hui HAN
1
;
Yanfeng ZHANG
1
;
Jie GAO
1
;
Lianming HUANG
1
;
Wenying LI
1
Author Information
1. 054000 河北省邢台，冀中能源邢台矿业集团总医院
- Publication Type:Journal Article
- Keywords:
Hyperbaric oxygen;
Cerebral infarction;
miR-153-3p;
Apoptosis;
Inflammation reaction
- From:
Chinese journal of nautical medicine and hyperbaric medicine
2021;28(2):174-178
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effect and mechanism of hyperbaric oxygen (HBO) in alleviating infarction cerebral in rats via regulating miR-153-3p/Bcl-2 axis.Methods:A total of 32 Sprague-Dawley rats were divided into sham operation group, model group, HBO group, and HBO + mimic group according to the random number table method, with 8 rats in each group. The rat cerebral model was established by middle cerebral artery occlusion (MCAO) method. After 48 hours of reperfusion, the rats were euthanized, and their hippocampal and cortical tissues were collected to assess the brain edema and nerve function damage. The TUNEL assay was used to observe the cell apoptosis in rat hippocampus and cortex. The RT-PCR test was used to detect the expression level of miR-153-3p in the rat brain tissue. The Western blotting test was adopted to detect the protein expression level of rat brain tissue. The ELISA was used to detect the level of inflammatory factor in the rat brain tissue. The luciferase reporter assay was used to detect the transcription activity of Bcl-2. The RT-PCR test was to detect the expression level of Bcl-2 mRNA in PC-12 cells.Results:Compared with the sham operation group, the expression level of miR-153-3p in the brain tissue of rats in the model group after MCAO treatment was significantly increased, and the expression level of miR-153-3p induced by MCAO was reduced after HBO treatment, but the expression level changing of miR-153-3p in the hyperbaric oxygen + mimic group was obviously reversed after the intervention of mimic-miR-153-3p, and the differences were all statistically significant ( P<0.05). Compared with the sham operation group, the neurological damage score and brain water content in the model group increased, and the score and content decreased after HBO treatment, but the effect of HBO was significantly mitigated after miR-153-5p overexpression; and the differences were all statistically significant ( P<0.05). Compared with the model group, the levels of IL-6, CRP, and TNF-α in the brain tissue of rats in the HBO group were significantly reduced, while the up-regulation of miR-153-3p increased the expression levels of IL-6, CRP, and TNF-α; and the differences were all statistically significant ( P<0.05). When the expression of miR-153-3p in rat PC-12 cells was up-regulated, the fluorescence and transcriptional activity of Bcl-2 were significantly reduced, the expression of miR-153-3p was up-regulated, and the level of Bcl-2 mRNA was reduced; the differences were all statistically significant ( P<0.05). Conclusion:Hyperbaric oxygen can relieve brain edema by improving the brain cell apoptosis and inflammatory reaction induced by MCAO via regulating the miR-153-3p/Bcl-2 axis.
