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目的观察联合应用水蛭注射液后处理对脑缺血损伤大鼠GSK-3β、eNOS蛋白表达的影响,以探讨其对脑缺血再灌注损伤的神经保护机制。方法 60只成年雄性SD大鼠,随机分为假手术组(S)、缺血-再灌注组(I/R)、缺血后处理组(P)、小剂量水蛭后处理组(S-H)、大剂量水蛭后处理组(L-H)、缺血后处理+大剂量水蛭组(P-H)等6组。采用线栓法制备大鼠局灶性脑缺血-再灌注损伤动物模型及缺血后处理模型,24 h后比较各组神经功能缺损评分,应用Western blot技术,观察GSK-3β、eNOS蛋白在大鼠缺血半暗带表达的变化。结果神经行为学评分:I/R组评分显著增高(P<0.01);与I/R组比较,其余各组评分均显著减少(P<0.01);其中P-H组评分最低(P<0.01)。GSK-3β/eNOS蛋白表达:与S组比较,I/R组GSK-3β含量上升,eNOS含量下降(P<0.01);与I/R组比较,其余各组GSK-3β表达显著下降、eNOS表达显著增高(P<0.01);P-H组此种表达趋势变化最明显(P<0.01)。结论水蛭注射液和缺血后处理可减轻神经功能缺损,下调GSK-3β、上调eNOS蛋白的表达,减轻脑缺血损害,两者联合具有协同神经保护作用,这种保护作用与水蛭的剂量可能有一定的关系。
Objective To observe the effect of combined application of leech injection on the expression of GSK-3β and eNOS in rats with cerebral ischemia injury, and to explore its neuroprotective mechanism on cerebral ischemia-reperfusion injury. Methods Sixty adult male Sprague-Dawley rats were randomly divided into four groups: sham operation group (S), ischemia / reperfusion group (I / R), ischemic postconditioning group (P), low dose leech postconditioning group High-dose leeches aftertreatment group (LH), ischemic postconditioning + high-dose leeches group (PH) and other 6 groups. The animal model of focal cerebral ischemia-reperfusion injury and ischemic postconditioning model were established by thread occlusion method. After 24 h, the neurological deficit score of each group was compared. Western blot was used to observe the expression of GSK-3β and eNOS protein Changes of ischemic penumbra in rats. Results Neurobehavioral score: The score of I / R group was significantly higher (P <0.01). Compared with I / R group, the scores of other groups were significantly decreased (P <0.01). The score of P-H group was the lowest (P <0.01). The GSK-3β / eNOS protein expression in I / R group was significantly higher than that in S group (P <0.01). GSK-3βexpression in I / R group was significantly lower than that in I / R group (P <0.01). In PH group, the expression trend of this expression was the most obvious (P <0.01). Conclusions Both Shuizhi injection and ischemic postconditioning can reduce neurological deficit, down-regulate GSK-3β, upregulate the expression of eNOS protein and alleviate cerebral ischemic damage. The combination of these two treatments has synergistic neuroprotective effect. This protective effect may be related to the dose of leech Have a certain relationship.