The interference of picrosideⅡ on the expressions of Caspase-3 and PARP following cerebral ischemia reperfusion injury in rats
- VernacularTitle:胡黄连苷Ⅱ对大鼠脑缺血/再灌注损伤Caspase-3和PARP表达的影响
- Author:
Qin LI
;
Yunliang GUO
;
Zhen LI
;
Xinying XU
- Publication Type:Journal Article
- Keywords:
picrosideⅡ;
cerebral ischemia;
reperfusion injury;
Caspase-3;
PARP;
apoptosis;
rats
- From:
Chinese Pharmacological Bulletin
2010;26(3):342-345
- CountryChina
- Language:Chinese
-
Abstract:
Aim To explore the effect of picrodideⅡ on the expressions of Caspase-3 and poly ADP-ribose polymerase (PARP) in brain tissue following cerebral ischemic reperfusion injury in rats.Methods The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in rats. PicrodideⅡ (10 mg·kg~(-1)) and salvianic acid A sodium (10 mg·kg~(-1)) were injected from tail vein for treatment. The neurological function was evaluated with Bederson's test and the cerebral infarction volume was observed with tetrazolium chloride (TTC) staining.The brain structure was observed by hematoxylin-eosin (HE) staining and the apoptosis was counted by TUNEL immunofluorescence assay. The expressions of Caspase-3 and PARP were detected with immunohistochemical and enzyme linked immunosorbent assay.Results After ischemia 2 h and reperfusion 22 h, the rats showed neurological function deficit and cerebral infarction in ischemic hemisphere. The expressions of Caspase-3 and PARP and the number of apoptotic cells in brain tissue increased compared with those in the sham operative group (P <0.05). In picroside and salvianic acid A sodium groups, the Bederson's scores and cerebral infarction volume, the expressions of Caspase-3 and PARP and the number of apoptosis cells were lower than those in the negative control group (P <0.05). While there was no significant difference in five indexes metioned above between picroside group and salvianic acid A sodium group (P >0.05).Conclusion PicrosideⅡ might reduce the expressions of Caspase-3 and PARP to inhibit the neuronal apoptosis induced by cerebral ischemia reperfusion injury and improve the neurological function of rats.
