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人尿激肽原酶对急性局灶性脑缺血再灌注损伤大鼠细胞凋亡的影响 被引量:3

Effects of human urinary kallikrein on cell apoptosis of rats with acute focal cerebral ischemia- reperfnsion injury
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摘要 目的研究人尿激肽原酶(HUK)对大鼠急性局灶性脑缺血再灌注(FCIR)损伤后细胞凋亡数量及B细胞淋巴瘤/白血病-2(Bcl-2)、Bcl-2联合X蛋白(Bax)蛋白表达的影响。方法84只雄性SD大鼠分为假手术组(12只)、脑缺血再灌注(IR)组(36只)、HUK处理组(36只),IR组和HUK处理组剩余大鼠又按照再灌注时间6h、12h、24h、72h、168h分为5个亚组(均为6只)。建立大鼠大脑中动脉FCIR模型。假手术组、IR组及HUK处理组中各取6只SD大鼠用于测定梗死体积,其余大鼠用于观察神经功能缺陷评分、TUNEL法及免疫组化检测凋亡细胞数量及凋亡蛋白Bcl-2、Bax的表达。结果HUK处理组神经功能缺陷评分、梗死灶体积、除168h亚组外的各时间点的凋亡细胞数及Bax蛋白表达均显著少于IR组(P〈0.05),除168h亚组外的各时间点的Bcl-2蛋白表达均显著高于瓜组(P〈0.05)。结论HUK对FCIR后的脑组织起保护作用,其机制可能为损伤后3d内通过上调Bcl-2、下调Bax蛋白表达来抑制细胞凋亡。 Objective To study the effects of human urinary kallikrein (HUK) on the number of apoptotic cells and the expressions of Bcl-2 and Bax proteins in rats after focal cerebral iscbemia and reperfusion (FCIR) injury. Methods Eighty-four Spraque-Dawley (SD) male rats were randomly divided into sham-operated group (n=12), iscbemia-reperfusion group (n=36), and HUK-treated group (n=36). Transient focal cerebral iscbemia models were established by middle cerebral artery occlusion. Six rats were chosen from sham-operated group, iscbemia-reperfusion group, and HUK-treated group for measuring infarct sizes. The rest were used to evaluate neurologic function impairment and measure the number of apoptotic cells and Bcl-2 or Bax protein positive cells in cerebral cortex with TUNEL and immunohistochemistry. The latter 2 groups were subdivided into 6, 12, 24, 72, 168 h reperfusion groups (each n=6). Results The neurologic function impairment score, the infarct sizes, the apoptotic cells and the expression of Bax protein of HUK-treated group at different time points (except 168 h group) significantly decreased compared with those ofischemia-reperfusion group (P〈0.05). The expression of Bcl-2 protein of HUK-treated group at different time points (except 168 h group) remarkably increased compared with that of ischemia-reperfusion group (P〈0.05). Conclusions HUK can exert a protection against FCIR injury, maybe through up-regulating Bcl-2 and down-regulating Bax protein in the initial 3 d of FCIR injury to decrease the number of apoptotic cells
出处 《中华神经医学杂志》 CAS CSCD 2008年第3期273-277,共5页 Chinese Journal of Neuromedicine
关键词 局灶性脑缺血再灌注损伤 人尿激肽原酶 细胞凋亡 Focal cerebral ischemia-reperfusion injury Human urinary kallikrein Apoptosis
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  • 1井明艳,孙建义.激肽释放酶的研究进展[J].中国抗生素杂志,2005,30(3):187-192. 被引量:4
  • 2李晓莉,侯永敏,苗丕渠.治疗急性脑梗死新药——凯力康[J].中国处方药,2005,4(11):69-72. 被引量:36
  • 3Xia CF,Yin H,Yao YY,et al.Kallikrein protects against ischemic stroke by inhibiting apoptosis and inflammation and promoting angiogenesis and neurogenesis[J].Hum Gene Ther,2006,17(2):206-219. 被引量:1
  • 4Chao J,Chao L.Experimental therapy with tissue kallikrein against cerebral ischemia[J].Front Biosci,2006,11:1323-1327. 被引量:1
  • 5Wang CX,Yang Y,Yang T,et al.A focal embolic model of cerebral ischemia in rats:introduction and evaluation[J].Brain Res Brain Res Protoc,2001,7(2):115-120. 被引量:1
  • 6Chao J,Chao L.Kallikrein-kinin in stroke,cardiovascular and renal disease[J].Exp Physiol,2005,90(3):291-298. 被引量:1
  • 7Emanuelia C,Madeddu P.Human tissue kallikrein:a new bullet for the treatment of ischemia[J].Curr Pharm Des,2003,9(7):589-597. 被引量:1
  • 8Suzuki S,Gerhold LM,Bottner M,et al.Estradiol enhances neurogenesis following ischemic stroke through estrogen receptors alpha and beta[J].J Comp Neurol,2007,500(6):1064-1075. 被引量:1
  • 9Yonemori F,Yamaguchi T,Yamada H,et al.Spatial cognitive performance after chronic focal cerebral ischemia in rats[J].J Cereb Blood Flow Metab,1999,19(5):483-494. 被引量:1
  • 10Jolkkonen J,Puurunen K,Rantakomi S,et al.Behavioral effects of the alpha (2)-adrenoceptor antagonist,atipamezole,after focal cerebral ischemia in rats[J].Eur J Pharmacol,2000,400(2-3):211-219. 被引量:1

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