Protective effect and Bcl-2 expression of salvia miltiorrhiza pretreatment on retinal ischemia-reperfusion injury
10.11659/jjssx.04E015052
- VernacularTitle:丹参预处理对大鼠视网膜缺血再灌注损伤的作用及对Bcl-2表达的影响
- Author:
Hui CHENG
;
Zhaoxia SUN
;
Yuze SONG
- Publication Type:Journal Article
- Keywords:
salvia miltiorrhiza;
retinal ischemia-reperfusion injury;
Bcl-2
- From:
Journal of Regional Anatomy and Operative Surgery
2016;(1):17-20
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the protective effect and Bcl-2 expression of salvia miltiorrhiza pretreatment on retinal ischemia-reperfu-sion injury ( RIRI) . Methods One hundred and thirty two Wistar rats were randomly divided into the normal control group, the ischemia-reperfusion group and the salvia miltiorrhiza pretreatment group. The model of retinal ischemia-reperfusion injury was constructed by increas-ing the intraocular pressure. The ischemia-reperfusion and salvia miltiorrhiza pretreatment group were divided into five subgroups according to the different reperfusion time (6 h, 12 h, 24 h, 48 h and 72 h). Observe the histological changes in retina by HE staining. The SABC ( strept avidin-biotin complex) and Western-blot were used to measure changes of Bcl-2 protein levels in retinal. Results The positive ex-pression of Bcl-2 protein was weak in normal group. In the ischemia-reperfusion group and salvia miltiorrhiza pretreatment group, the expres-sion of Bcl-2 protein began to increase at 6 hours after reperfusion, reached the peak at 24 hours after reperfusion, began to decrease at 48 hours after reperfusion, and started to weaken at 72 hours after reperfusion. The variation tendency of the two groups were the same, however, the expression of Bcl-2 was significantly stronger in the salvia miltiorrhiza pretreatment group compared with ischemia-reperfusion group, and there was significant difference between the two groups (P<0. 01). Conclusion Salvia miltiorrhiza pretreatment can protect the retina by reducing retinal ganglion cells apoptosis in retinal ischemia-reperfusion injury. The mechanism may be achieved by regulating the expression of Bcl-2 protein.
