CAJ | 학술논문

目的观察人尿激肽原酶(HUK)对局灶性脑缺血再灌注损伤大鼠神经细胞凋亡及Caspase-3表达的影响. 方法 66只SD大鼠按随机数字表法分为假手术组(n=6)、缺血再灌注损伤组和HUK处理组,后两组又按不同观察时间点分为再灌注6h、12h、24 h、72 h、168 h共5个亚组(n=6).缺血再灌注损伤组和HUK处理组采用线栓法建立大鼠大脑中动脉局灶性脑缺血再灌注损伤模型,HUK处理组按浓度17.5×10-3PNAU/mL,1.0 mL/kg,于再灌注后3h尾静脉注射给药,1次/d.采用TUNEL法及免疫组化染色检测各组大鼠脑组织中凋亡细胞及Caspase-3阳性细胞的数量变化. 结果脑缺血再灌注损伤后6h即有细胞凋亡,于24 h达到高峰,至168 h仍可见凋亡细胞.Caspase-3阳性细胞表达均于再灌注24 h达高峰,至168 h仍有较多表达.除168 h时间点外,其余各时间点HUK处理组大鼠神经细胞凋亡数量、Caspase-3阳性细胞数量均明显低于缺血再灌注损伤组,差异均有统计学意义(P＜0.05). 结论 HUK在大鼠局灶性脑缺血再灌注损伤早期(6～72h)时能抑制细胞凋亡,推测与其减少Caspase-3的表达有关.
목적 관찰인뇨격태원매(HUK)대국조성뇌결혈재관주손상대서신경세포조망급Caspase-3표체적영향. 방법 66지SD대서안수궤수자표법분위가수술조(n=6)、결혈재관주손상조화HUK처리조,후량조우안불동관찰시간점분위재관주6h、12h、24 h、72 h、168 h공5개아조(n=6).결혈재관주손상조화HUK처리조채용선전법건립대서대뇌중동맥국조성뇌결혈재관주손상모형,HUK처리조안농도17.5×10-3PNAU/mL,1.0 mL/kg,우재관주후3h미정맥주사급약,1차/d.채용TUNEL법급면역조화염색검측각조대서뇌조직중조망세포급Caspase-3양성세포적수량변화. 결과 뇌결혈재관주손상후6h즉유세포조망,우24 h체도고봉,지168 h잉가견조망세포.Caspase-3양성세포표체균우재관주24 h체고봉,지168 h잉유교다표체.제168 h시간점외,기여각시간점HUK처리조대서신경세포조망수량、Caspase-3양성세포수량균명현저우결혈재관주손상조,차이균유통계학의의(P＜0.05). 결론 HUK재대서국조성뇌결혈재관주손상조기(6～72h)시능억제세포조망,추측여기감소Caspase-3적표체유관.
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.