论文部分内容阅读
目的探讨原花青素(procyanidin,PC)对脑缺血再灌注损伤大鼠Caspase-3和Caspase-9活性的影响。方法将大鼠随机分为假手术组、缺血再灌注组、PC低剂量治疗组和PC高剂量治疗组,线栓法建立局灶性脑缺血再灌注模型。采用四肽酶底物法检测脑缺血90 min再灌注24 h大鼠Caspase-3和Caspase-9活性,进行神经症状评分,2,3,5-三苯基氯化四氮唑(TTC)染色和HE染色观察脑梗塞体积及病理形态学变化。结果脑缺血再灌注24 h,缺血再灌注组Caspase-3和Caspase-9活性增加,与假手术组比较,差异具有显著性(均P<0.05);与缺血再灌注组比较,PC高、低剂量治疗组均显著减少Caspase-3和Caspase-9活性,高、低剂量组之间差异亦具有显著性(P<0.05)。PC高、低剂量治疗组神经功能缺失评分较缺血再灌注组降低(P<0.05)。PC高、低剂量治疗组脑梗死体积较缺血再灌注组减小,高、低剂量组之间差异具有显著性(P<0.05)。PC高、低剂量治疗组脑组织缺血损伤病理学改变明显轻于缺血再灌注组,PC高剂量治疗组缺血改变亦轻于低剂量治疗组。结论PC对缺血再灌注脑损伤具有保护作用,其机制可能与减少Caspase-3和Caspase-9活性,抗凋亡有关。
Objective To investigate the effects of procyanidin (PC) on the activity of Caspase-3 and Caspase-9 in rats with cerebral ischemia-reperfusion injury. Methods The rats were randomly divided into sham-operated group, ischemia-reperfusion group, PC low-dose treatment group and high-dose PC treatment group. The model of focal cerebral ischemia-reperfusion was established by thread occlusion. The activity of Caspase-3 and Caspase-9 in rats after cerebral ischemia 90 min and 24 h after reperfusion was detected by tetrapeptase substrate method. The neurological symptom scores, 2,3,5-triphenyltetrazolium tetrazolium (TTC) Staining and HE staining were used to observe the infarct volume and pathological changes. Results Compared with the sham-operation group, the changes of Caspase-3 and Caspase-9 activity in ischemia-reperfusion group were significantly increased at 24 h after cerebral ischemia-reperfusion (all P <0.05) The high and low dose treatment groups significantly reduced the activity of Caspase-3 and Caspase-9, and the difference between the high and low dose groups was also significant (P <0.05). The score of neurological deficit in PC high and low dose treatment groups was lower than that in ischemia / reperfusion group (P <0.05). The volume of cerebral infarction in PC high and low dose treatment groups was smaller than that in ischemia / reperfusion group, and there was significant difference between high and low dose groups (P <0.05). The pathological changes of ischemic brain tissue in high and low dose PC groups were significantly lighter than those in ischemia / reperfusion group. The ischemic changes in PC high dose group were also lighter than those in low dose group. Conclusions PC has a protective effect on brain injury induced by ischemia-reperfusion. The mechanism may be related to the decrease of Caspase-3 and Caspase-9 activity and anti-apoptosis.