Protective function of human urinary kallidinogenase in rats after focal cerebral ischemic reperfusion and its effect on caspase-3 expression
10.3760/cma.j.issn.1671-8925.2012.09.006
- VernacularTitle:人尿激肽原酶对大鼠局灶性脑缺血再灌注损伤的保护作用及对Caspase-3表达的影响
- Author:
Ling-Li LU
1
;
Zhen-Hua LIU
;
Hui-Fang XIE
;
Xue-Ping SONG
;
Ji-Peng WEI
Author Information
1. 南方医科大学珠江医院
- Keywords:
Human urinary kallidinogenase;
Cerebra ischemia-reperfusion injury;
Apoptosis
- From:
Chinese Journal of Neuromedicine
2012;11(9):887-890
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of human urinary kallidinogenase (HUK) on neural cell apoptosis in rats after focal cerebral ischemia-reperfusion (FCIR) injury and on Caspase-3 expression.Methods Sixty-six SD rats were randomly divided into sham-operated group (n=6),ischemic-reperfusion group and HUK treatment group.The latter 2 groups were subdivided into 6,12,24,72 and 168 h reperfusion groups (n=6).Middle cerebral artery occlusion models of transient focal cerebral ischemia in the latter 2 groups were established by suture-occluded method. Rats of the HUK treatment group were given tail vein injection of HUK once daily at dosage of 17.5 ×10-3 PNAU/mL and at 1.0 mL/kg manner 3 h after reperfusion. The numbers of apoptotic cells and Caspase-3 positive cells in the cerebral cortex were evaluated with terminal dUTP nick end labeling (TUNEL) assay and immunohistochemistry. Results Cell apoptosis was noted 6 h after the focal cerebral ischemia-reperfusion,reaching its peak level at 24 h,and the apoptotic cells could still be seen at 168 h after the injury.And the expression of Caspase-3 positive cells peaked at 24 h after the injury,and high expression was still noted at 168 h after the injury. The levels of apoptotic cells and the expression of Caspase-3 positive cells in HUK treatment group at different time points (except for 168 h subgroup) decreased significantly as compared with those in ischemic-reperfusion group (P＜0.05). Conclusion HUK may decrease the number of apoptotic cells in the initial 72 h of FCIR injury by down-regulating the Caspase-3 expression.
