Effect of Shenxiong Injection on the expression of X-box binding protein 1 of endoplasmic reticulum stress following cerebral ischemia-reperfusion injury in rats
10.3760/cma.j.issn.1673-4165.2009.11.005
- VernacularTitle:参芎注射液对大鼠脑缺血再灌注后内质网应激相关分子X盒结合蛋白1表达的影响
- Author:
Zhibo ZHANG
;
Lu TANG
;
Xu PENG
- Publication Type:Journal Article
- Keywords:
cerebral ischemia;
reperfusion injury;
endoplasmic reticulum;
DNA-binding proteins;
shenxiong injection;
rats
- From:
International Journal of Cerebrovascular Diseases
2009;17(11):844-848
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effect of Shenxiong injection on the changes of brain X-box binding protein 1 (XBP1) gene expression following cerebral ischemia-reperfusion in rats and to investigate its neuroprotective effect and mechanisms. Methods One hundred forty-four male SD rats were randomly assigned to sham-operation, saline control and Shenxiong groups. A rat model of middle cerebral artery occlusion was induced using the suture method. Shenxiong injection 33.3 ml/kg was injected intraperitoneally during the reperfusion in the Shenxiong group. The same volume of saline was injected intraperitoneally in the saline control group. The animals were sacrificed at 6, 12, 24, and 72 hours after the reperfusion.Meanwhile, immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR) were used respectively to detect the expressions of XBP1 protein and mRNA in the cerebral ischemic areas. TUNEL was used to detect neuronal apoptosis. Results The levels of XBP1 protein and mRNA increased after the reperfusion, and it reached the peak at 12 hours; both the numbers of apoptotic cells and neurological scores in the Shenxiong group were lower than those in the saline control group at 6, 12, 24, and 72 hours after the reperfusion (all P ＜0.01); the levels of XBP1 and mRNA at 6, 12, and 24 hours after the reperfusion were alsosignificantly lower than those in the saline control group (all P ＜ 0.01). Conclusions Shenxiong injection may have certain inhibition on the endoplasmic reticulum stress activated XBP1 pathway induced by cerebral ischemia-reperfusion.
