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还原型谷胱甘肽对大鼠肺缺血再灌注后肺细胞凋亡的影响 被引量:4

Effects of reduced glutahione on apoptosis induced by pulmonary ischemia/reperfusion in rat
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摘要 目的探讨还原型谷胱甘肽对大鼠肺缺血再灌注后肺细胞凋亡的影响。方法雄性清洁级大鼠72只,随机分为3组,假手术组(shamoperation,SO)(n=24)、缺血再灌注组(ischemia-reperfusion,IR)(n=24)、还原型谷胱甘肽治疗组(reducedglutathionegroup,RG)(n=24),每组随机分为4个亚组(n=6)。参照Okada的方法,建立原位阻断肺门的大鼠肺缺血再灌注损伤模型。RG组在缺血前5min注射还原型谷胱甘肽800mg/kg,IR组与SO组注射等量的生理盐水。缺血45min、再灌注后1,2及4h4个时点处死大鼠进行指标测定。凋亡细胞的检测使用TUNEL技术;Bcl-2蛋白表达采用SP法测定;采用ELISA法测定10%肺匀浆中TNF-α含量。结果大鼠肺缺血再灌注损伤后,IR组肺组织细胞凋亡明显高于SO组和RG组(均P<0.01),再灌注后RG组Bcl-2蛋白表达明显高于SO组和IR组,TNF-α含量在IR组缺血再灌注后含量明显增加,较SO,RG组显著增高(P<0.01)。结论还原型谷胱甘肽能减少肺缺血再灌注后肺细胞的凋亡。 Objective To observe the effects of reduced glutathione on apoptosis induced by pulmonary isehemia-reperfusion in rats . Methods Seventy-two male SD rats were randomly divided into 3 groups: the sham groups(SO, n=24); theischemia-repeffusion group(IR, n = 24) ;the reduced glutathione-treated group(RG, n = 24),and each group was randmnly subdivided into 4 subgroup( n = 6). IR injury was in duced by in situ pulmonary hilum occlusion. The group RG was treated by reduced glutathione (800 mg/kg) 5 rains before ischemia, while other two groups were treated by normal saline.Pulmonary tissues were obtained 45 rains after ischemia and 1, 2, 4 h after repeffusion. Apoptosis was investigated by TUNEL; The expression of Bcl-2 were measured by inununobistochemical technique(SP);ELISA was used to determine the level of tumor necrosis factor-alpha (TNF-α).Results In IR group,pulmonary apoptosis was significantly higher increased than that in the SO and RG group( P 〈 0.01)after ischemia-repefusion. In RG group, expression of Bcl-2 was significantly higher than that in the S and IR group ( P 〈 0.01) after ischemia- repeffusion. TNF - α in IR group was significantly higher than that in the SO and RG group. Conclusion Reduced glutathione can decrease pulmonary apoptosis after ischemia-repeffusion.
出处 《广东医学》 CAS CSCD 北大核心 2006年第8期1133-1135,共3页 Guangdong Medical Journal
基金 贵州省科技计划项目(编号:黔科合专字[2003]33-3)
关键词 缺血/再灌注 还原型谷胱甘肽 细胞凋亡 Ischemia-reperfusion Lung Reduced glutathione Apoptosis
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参考文献8

  • 1JIN Q,KANG C,SOH Y,et al.Tetrandrine cytotoxicity and its dual effect on oxidative stress-induced apoptosis through modulating cellular redox states in Neura 2a mouse neuroblastoma cells[J].Life Sci,2002,71(17):2053-2066.
  • 2OKADA M,YAMASHITA C,OKADA A.Contribution of endothelin-1 to warm ischemia/reperfusion injury of the rat lung[J].Am J Respir Crit Care Med,1995,152(6 pt1):2105-2110.
  • 3STAMMBERGER U,GASPERT A,HILLINGER S,et al.Apoptosis induced by ischem is And reperfusion in experimental lung transplantation[J].Ann Thorac Surg,2000,69(5):1532-1536.
  • 4谢东甫,秦雄,徐志飞.大鼠肺缺血再灌注损伤引起肺细胞的凋亡[J].第二军医大学学报,2004,25(3):295-297. 被引量:2
  • 5LEICHTWEIS S,JI L L.Glutathione deficiency intensifies ischemiareperfusion induced cardiacdysfunction and oxidative stress[J].Acta Physiol Scand,2001,172(1):1-10.
  • 6RAHMAN I.Regulation of nuclear factor-kappaB,activator proteirr-l and glutathione levels by tumor necrosis factor-alpha and dexamethasone in alveolar epithelial cells[J].Biochem Pharmacol,2000,60(8):1041-1049.
  • 7JIN Q,KANG C,SOH Y,et al.Tetrandrine cytotoxicit and its dual effect on oxidative stress-induced apoptosis through modulating cellular redox states in Neura 2a mouse neuroblastoma cells[J].Life Sci,2002,71(17):2053-2066.
  • 8MATSUSHITA H,MORISHITA R,NATA T,et al.Hypoxia induced endothelial apoptosis through nuclear factorkappaB(NF-kappaB)-mediated Bcl-2 suppression:in vivo evidence of the importance of NFkappaB in endothelialcell regulation[J].Cite Res,2000,86(9):974-981.

二级参考文献11

  • 1[1]Thompson CB.Apoptosis in the pathogenesis and treatment of disease[J].Science,1995,267(5203):1456-1462.
  • 2[2]Buttke TM,Sandstrom PA.Oxidative stress as a mediator of apoptosis[J].Immunol Today,1994,15(1):7-10.
  • 3[3]Ikeda H,Suzuki Y,Suzuki M,et al.Apoptosis is a major mode of cell death caused by ischaemia and ischaemia/reperfusion injury to the rat intestinal epithelium[J].Gut,1998,42(4):530-537.
  • 4[4]Kerr JFR,Wyllie AH,Currie AR.Apoptosis:a basic biological phenomenon with wide-ranging implications in tissue kinetics[J].Br J Cancer,1972,26(4):239-257.
  • 5[5]Bursch W,Paffe S,Putz B,et al.Determination of the length of the histological stages of apoptosis in normal liver and in altered hepatic foci of rats[J].Carcinogenesis,1990,11(5):847-853.
  • 6[6]Noda T,Iwakiri R,Fujimoto K,et al.Programmed cell death induced by ischemia-reperfusion in rat intestinal mucosa[J].Am J Physiol,1998,274(2 Pt 1):G270-G276.
  • 7[7]Sasaki H,Matsuno T,Nakagawa K,et al.Induction of apoptosis during the early phase of reperfusion after rat liver ischemia[J].Acta Med Okayama,1997,51(6):305-312.
  • 8[8]Gottlieb RA,Burleson KO,Kloner RA,et al.Reperfusion injury induces apoptosis in rabbit cardiomyocytes[J].J Clin Invest,1994,94(4):1621-1628.
  • 9[9]Shah KA,Shurey S,Green CJ.Apoptosis after intestinal ischemia-reperfusion injury:a morphological study[J].Transplantation,1997,64(10):1393-1397.
  • 10[10]Stammberger U,Gaspert A,Hillinger S,et al.Apoptosis induced by ischemia and reperfusion in experimental lung transplantation[J].Ann Thorac Surg,2000,69(5):1532-1536.

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