邵春红 胡德耀 薛春生
摘 要:目的探讨吡那地尔(Pinacidil)预处理(preconditioning,PC)对失血性休克大鼠保护作用的机制。方法(1)大鼠90只,随机分为正常组(N组,10只)、对照组(C组,40只)和预处理组(PC组,40只),PC组大鼠用Pinacidil进行预处理,24h后将对照组和预处理组大鼠复制成失血性休克模型,用Westernblot方法观察不同时相点大鼠心肌组织细胞型磷脂酶A2(cPLA2)的表达变化;(2)大鼠60只,随机分为对照组(C组,30只)和预处理组(PC组,30只),PC组大鼠用Pinacidil进行预处理,然后分别在24,48,72h3个不同时间点将两组大鼠复制成失血性休克模型,用Westernblot方法观察PC对大鼠心肌和肝脏组织热休克蛋白70(hsp70)表达的影响。结果(1)PC组心肌组织cPLA2的表达较弱,而C组表达很强;(2)C组hsp70表达很弱或检测不到,PC组心肌和肝脏hsp70表达很强,24h达到高峰,48h和72h逐渐减弱。结论Pinacidil预处理可能是通过诱导hsp70过度表达和抑制PLA2的表达保护"休克细胞",从而保护失血性休克大鼠的心肌和肝脏组织。
关键词:休克,出血性;热休克蛋白质类;磷脂酶A2;预处理
分类号:R65 文献标识码:A
Effects of Pinacidil preconditioning on hsp70 and cPLA2 expression in hemorrh agic shock rats
SHAO Chunhong(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
HU Deyao(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
XUE Chunsheng(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
Abstract:Objective To investigate the mechanisms of Pinacidil prec onditioning protection of hemorrhagic shock rats. Methods The rats were divided into 3 groups: a normal group ( n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditio ning was processed 24 h before making the hemorrhagic shock model. The cPLA2 expression in myocardium was observed at different time points with western blot; Pinacidil preconditioning was processed 24, 48 and 72 h before making th e hemorrhagic shock model to observe hsp70 expression in myocardium and liver tissue with western blot. Results Pinacidil preconditioning could increase hsp70 expres sion and decrease cPLA2 expression. Conclusions Pinacidil preconditioning protects "shock cell" by inducing hsp70 overexpression and inhibiting cPLA2 expression, which is re sponsible for protecting myocardial and liver tissues of the hemorrhagic shock rats.
Keywords:Shock, hemorrhagic; Heat-shock proteins; Phos phlipases A2; Preconditioning
作者单位:邵春红(400042 重庆,第三军医大学附属大坪医院野战外科研究所二室)
胡德耀(400042 重庆,第三军医大学附属大坪医院野战外科研究所二室)
薛春生(重庆医科大学药理教研室)
参考文献:
[1]邵春红,胡德耀,薛春生. 吡那地尔预处理对低血容量性休克大鼠心肌离子泵影响的实验研究. 中国危重病急救医学, 2000, 12:660-662.
[2]陆松敏,王成英,刘建仓,等. 失血性休克条件下磷脂酶A2(PLA2)和细胞膜脂流动性的改变. 中国病理生理杂志, 1994, 10:73-75.
[3]Prasad MR, Popescu LM, Moraru II, et al.Role of phospholipase A2 an d C in myocardial ischemic reperfusion injury. Am J Physiol, 1991,260 (3 Pt 2):H877-H883.
[4]Lefer AM. Significance of lipid mediators in shock states. Circulator y Shock, 1989, 27:3-12.
[5]Jaattela M. Overexpression of major heat shock protein hsp70 inhibit s tumor necrosis factor-induced activation of phospholipase A2. J Immunol, 1 993, 151:4286-4294.
[6]Villar J, Edelson JD, Post M, et al. Induction of heat stress protei ns is associated with decreased mortality in an animal model of acute lung inj ury. Am Rev Respiv Dis, 1993, 147:177-181.
[7]Baler R, Dahl G, Voellmy R. Activation of human heat shock genes is accompanied by oligomerization, modification, and rapid translocation of heat shock transcription factor HSF1. Mol Cell Biol, 1993, 13:2486-2492.
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摘 要:目的探讨吡那地尔(Pinacidil)预处理(preconditioning,PC)对失血性休克大鼠保护作用的机制。方法(1)大鼠90只,随机分为正常组(N组,10只)、对照组(C组,40只)和预处理组(PC组,40只),PC组大鼠用Pinacidil进行预处理,24h后将对照组和预处理组大鼠复制成失血性休克模型,用Westernblot方法观察不同时相点大鼠心肌组织细胞型磷脂酶A2(cPLA2)的表达变化;(2)大鼠60只,随机分为对照组(C组,30只)和预处理组(PC组,30只),PC组大鼠用Pinacidil进行预处理,然后分别在24,48,72h3个不同时间点将两组大鼠复制成失血性休克模型,用Westernblot方法观察PC对大鼠心肌和肝脏组织热休克蛋白70(hsp70)表达的影响。结果(1)PC组心肌组织cPLA2的表达较弱,而C组表达很强;(2)C组hsp70表达很弱或检测不到,PC组心肌和肝脏hsp70表达很强,24h达到高峰,48h和72h逐渐减弱。结论Pinacidil预处理可能是通过诱导hsp70过度表达和抑制PLA2的表达保护"休克细胞",从而保护失血性休克大鼠的心肌和肝脏组织。
关键词:休克,出血性;热休克蛋白质类;磷脂酶A2;预处理
分类号:R65 文献标识码:A
Effects of Pinacidil preconditioning on hsp70 and cPLA2 expression in hemorrh agic shock rats
SHAO Chunhong(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
HU Deyao(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
XUE Chunsheng(Institute of Surgery, Daping Hospital, the Third Military Medical University, Chongqing 400042, China)
Abstract:Objective To investigate the mechanisms of Pinacidil prec onditioning protection of hemorrhagic shock rats. Methods The rats were divided into 3 groups: a normal group ( n=10), a control group (n=40) and a preconditioning group (n=40). Pinacidil preconditio ning was processed 24 h before making the hemorrhagic shock model. The cPLA2 expression in myocardium was observed at different time points with western blot; Pinacidil preconditioning was processed 24, 48 and 72 h before making th e hemorrhagic shock model to observe hsp70 expression in myocardium and liver tissue with western blot. Results Pinacidil preconditioning could increase hsp70 expres sion and decrease cPLA2 expression. Conclusions Pinacidil preconditioning protects "shock cell" by inducing hsp70 overexpression and inhibiting cPLA2 expression, which is re sponsible for protecting myocardial and liver tissues of the hemorrhagic shock rats.
Keywords:Shock, hemorrhagic; Heat-shock proteins; Phos phlipases A2; Preconditioning
作者单位:邵春红(400042 重庆,第三军医大学附属大坪医院野战外科研究所二室)
胡德耀(400042 重庆,第三军医大学附属大坪医院野战外科研究所二室)
薛春生(重庆医科大学药理教研室)
参考文献:
[1]邵春红,胡德耀,薛春生. 吡那地尔预处理对低血容量性休克大鼠心肌离子泵影响的实验研究. 中国危重病急救医学, 2000, 12:660-662.
[2]陆松敏,王成英,刘建仓,等. 失血性休克条件下磷脂酶A2(PLA2)和细胞膜脂流动性的改变. 中国病理生理杂志, 1994, 10:73-75.
[3]Prasad MR, Popescu LM, Moraru II, et al.Role of phospholipase A2 an d C in myocardial ischemic reperfusion injury. Am J Physiol, 1991,260 (3 Pt 2):H877-H883.
[4]Lefer AM. Significance of lipid mediators in shock states. Circulator y Shock, 1989, 27:3-12.
[5]Jaattela M. Overexpression of major heat shock protein hsp70 inhibit s tumor necrosis factor-induced activation of phospholipase A2. J Immunol, 1 993, 151:4286-4294.
[6]Villar J, Edelson JD, Post M, et al. Induction of heat stress protei ns is associated with decreased mortality in an animal model of acute lung inj ury. Am Rev Respiv Dis, 1993, 147:177-181.
[7]Baler R, Dahl G, Voellmy R. Activation of human heat shock genes is accompanied by oligomerization, modification, and rapid translocation of heat shock transcription factor HSF1. Mol Cell Biol, 1993, 13:2486-2492.
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