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皮质抑素对脓毒症大鼠心肌凋亡的影响 被引量:2

Effect of cortistatin on myocardium apoptosis in rats with sepsis
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摘要 目的:探讨皮质抑素对脓毒症大鼠心肌凋亡的影响。方法:SD雄性大鼠随机分为假手术对照组、脓毒症组、皮质抑素+脓毒症组。分别在盲肠结扎穿孔手术后18 h监测平均动脉压及心脏功能,腹主动脉取血处死大鼠,留取血清检测乳酸,留取心肌组织检测丙二醛(MDA)含量、caspase-3活性及p-JAK2、p-STAT3蛋白表达情况,病理切片进行TUNEL染色。结果:脓毒症大鼠表现出平均动脉压降低,心脏功能抑制和高乳酸特征,且心肌caspase-3活性升高,凋亡细胞数目增多及p-JAK2、p-STAT3蛋白表达水平升高。而预先给予皮质抑素可以改善脓毒症大鼠血流动力学及代谢特点,减轻心肌凋亡。结论:皮质抑素可以改善脓毒症介导的心肌凋亡,且这一作用与JAK2/STAT3信号通路相关。 Objective: To investigate the effect of cortistatin on myocardium apoptosis in rats with sepsis. Methods:Rats were randomly divided into 3 groups: control group,sepsis group and cortistatin + sepsis group. Mean arterial pressure( MAP) and cardiac function were monitored 18 hours after CLP. Then blood was taken from the aortaventralis to sacrifice the rat and determined serum lactic acid. Myocardial MDA content was measured and caspase-3 activity was determined by use of a colorimetric assay kit. Then western blot was used to test p-JAK2 and p-STAT3 protein expression. TUNEL staining was used to measure myocardial apoptosis. Results: Rats with sepsis exhibited a decreased MAP,inhibited heart function and characteristic of high lactic acid. The level of caspase-3 activity,number of myocardium apoptosis and the protein levels of p-JAK2 and p-STAT3 in rats with sepsis were elevated. Rat,pretreated with cortistatin,showed attenuation of blood flow dynamics,and metabolic anormalies as well as reduction of myocardium apoptosis induced by sepsis. Conclusions: Cortistatin may improve the myocardium apoptosis induced by sepsis by inhibiting JAK2 / STAT3 signaling pathway.
出处 《内科急危重症杂志》 2015年第1期61-63,共3页 Journal of Critical Care In Internal Medicine
关键词 皮质抑素 脓毒症 凋亡 JAK2/STAT3 Cortistatin Sepsis Apoptosis JAK2/STAT3
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  • 1杨朝坤,杨双强,谭松涛,汪斌,陈力.河豚毒素停搏液减轻大鼠心肌细胞内钙超载作用的实验研究[J].第三军医大学学报,2005,27(3):192-195. 被引量:9
  • 2杨双强,谭松涛,杨朝坤,汪斌,陈力.极化停搏液用于离体大鼠心脏保存的实验研究[J].重庆医科大学学报,2005,30(3):438-441. 被引量:8
  • 3夏正远,顾家珍,张遵严,翟中云,余金甫,黄海波,胡岚.体外循环下心肌缺血再灌注后血清心肌酶、SOD活性变化及复方丹参的应用[J].中华麻醉学杂志,1996,16(4):153-155. 被引量:24
  • 4Hattori R, Maulik N, Otani H, et al.Role of STAT3 in ischemia preconditioning[J]. J Mol Cell Cardiol, 2001,33( 11 ) : 1929-1936.
  • 5Omura T, Yoshiyama M, Ishikura F, et al.Myocardial ischemia activates the JAK-STAT pathway through angiotensin Ⅱ signaling in vivo myocardium of rats[J].J Mol Cell Cardiol, 2001,33(2) : 307-316.
  • 6Xuan Y T, Guo Y, Han H, et a l.An essential role of the JAK-STAT pathway in ischemic preconditioning[J]. Proc Natl Acad Sci USA, 2001,98 (16) : 9050-9055.
  • 7Schindler C W.Series introduction JAK-STAT signaling in human disease[J].J Clin Invest, 2002,109 (9) : 1133-1137.
  • 8Paradies G,Petrosillo G,Pistolese M,et al.Lipid peroxidation and alterations to oxidative metabolism in mitochondria isolated from rat heart subjected to ischemia and reperfusion[J].Free Radic Biol Med, 1999,27 ( 1-2 ) : 42-50.
  • 9Negoro S, Kunisada K, Fujio Y,et al.Activation of signal transducer and activator of transcription 3 protects cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress through the upregulation of manganese superoxide dismutase[J].Circulation, 2001,104(9 ):979-981.
  • 10Oshima Y,Fujio Y,Nakanishi T,et al.STAT3 mediates cardioprotection against ischemia/reperfusion injury through metallothionein induction in the heart[J]. Cardiovasc Res,2005,65(2) :428-435.

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