摘要
目的探讨大鼠整体低氧预处理(WHPC)对在体肺缺血再灌注(I/R)损伤的保护作用。方法用重复低氧5次建立大鼠WHPC模型,用无创微血管夹夹闭左肺门缺血45min后松开,再灌注180min,复制肺I/R模型。设立假手术(Sham)组、I/R组和WHPC+I/R组,每组SD大鼠10只。光镜下观察各组肺组织形态学变化,用免疫组织化学染色法检测肺组织细胞色素C的表达,TUNEL法检测肺组织细胞凋亡,并用非放射性荧光底物法检测肺组织蛋白激酶C(PKC)活性。结果与Sham组比较,I/R组肺组织出现明显损伤性形态学变化,肺组织细胞色素C表达及细胞凋亡指数显著增高(P<0.01);与I/R组比较,WHPC+I/R组形态学变化明显改善,肺组织细胞色素C表达及细胞凋亡指数均降低(P<0.05)。WHPC+I/R组肺组织PKC活性比Sham组和I/R组明显增高。结论 WHPC可减少肺组织细胞色素C表达,抑制细胞凋亡,对肺I/R损伤具有保护作用,该保护作用可能与WHPC上调PKC活性有关。
Objective To investigate the protective effect of whole-body hypoxic preconditioning (WHPC) on lung ischemia- reperfusion injury in rats. Methods Thirty rats were randomly divided into three groups (n = 10, respectively) : sham-operation group, I/R group and WHPCA-I/R group. WHPC rat model was established with 5 times of repetitive sublethal hypoxia. Pulmonary ischemia-reperfusion injury model was established by 45 rain of left hilar clamping followed by 180 min of reperfusion. Morpho- logical changes of lung tissue were detected by HE staining. Cytochrome C expression in lung tissue was assessed by immunohistochemical staining. TUNEL was used to determine apoptosis. Protein Kinase C (PKC) activity in lung tissue was assessed by Pep- Tag non-radioactive assay. Results Compared with sham-operation group,expression of cytochrome C and apoptosis index of I/R group were dramatically increased. These parameters were obviously restored in WHPCA-I/R group. Meanwhile, PKC activity in WHPCq-I/R group lung tissue increased significantly. Conclusion Whole-body hypoxie preconditioning in rats can alleviate pulmo- nary ischemia-reperfusion injury by reducing release of cytochrome C and apoptosis. This protective effect may be associated with increasing in PKC activity.
出处
《重庆医学》
CAS
CSCD
北大核心
2010年第15期1960-1962,共3页
Chongqing medicine
基金
贵州省优秀科技教育人才省长专项基金资助项目(S2003-9)
关键词
肺
缺血再灌注损伤
预处理
细胞凋亡
蛋白激酶C
lung
ischemia-reperfusion injury
hypoxic preconditioning
apoptosis
protein kinase C