Expression of Bcl-2 and Bax after cerebral ischemia-reperfusion injury in rats with hyperlipemia and the effect of scutellarin
10.16098/j.issn.0529-1356.2019.04.005
- Author:
Ying-Chun YANG
1
Author Information
1. Department of Anatomy, Fenyang College, Shanxi Medical University
- Publication Type:Journal Article
- Keywords:
B-cell lymphoma-2;
Bcl-2 assaciated X protein;
Cerebral ischemia-reperfusion injury;
Hyperlipemia;
Rat;
Scutellarin;
Western blotting
- From:
Acta Anatomica Sinica
2019;50(4):431-437
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effect of scutellarin after cerebral ischemia-reperfusion injury in rats with hyperlipemia, by observing the expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2 assaciated X protein (Bax) in cerebral cortex with hyperlipemia. Methods: After the rat model of hyperlipidemia was established, the focal cerebral ischemiareperfusion model in hyperlipemia rats was established with thread embolism of the middle cerebral artery. The neurobehavioral score was used to observe the symptoms of neurobehavioral injury. 2,3,5 -triphenyl tetrazolium chloride (TTC) staining was used to observe the cerebral infarct volume. HE staining was used to observe the pathological changes of brain tissue. Immunohistochemistry and Western blotting were used to observe the expressions of Bcl-2 and Bax. Results: Compared with the sham-operation group, the neurobehavioral scores,cerebral infarction volum and pathologic damage were significantly increased, the expressions of Bcl-2 was significantly lower, the expressions of Bax was significantly increased in ischemia-reperfusion group(P<0. 05). Compared with the saline group, the neurobehavioral scores, cerebral infarction volum and pathologic damage were significantly decreased, the expression of Bcl-2 was significantly increased, the expression of Bax was significantly decreased in scutellarin treatment group (P<0. 05). Conclusion: In cerebral ischemiareperfusion injury rats with hyperlipemia, scutellarin can alleviate cerebral ischemia-reperfusion injury by promoting the expression of Bcl-2 and inhibiting the expression of Bax.
