期刊文献+

老化心肌功能损害的机制研究:心肌Toll样受体4表达的随龄变化

Study on the mechanism of aging myocardial function: Change of myocardium Toll-like receptor 4 expression with age
下载PDF
导出
摘要 目的:探讨心肌Toll样受体4表达的随龄变化,寻找老化心肌损害的防治方法。 方法:以雌性成年(8~12周)及老龄BALB/C小鼠(20个月)为实验对象,用反转录-聚合酶链反应(Reverse transcription-polymerase chain reaction,RT-PCR)和免疫组化方法,对成年及老龄小鼠心肌Toll样受体4mRNA表达及蛋白表达进行检测。 结果:与成年小鼠相比,老龄小鼠心肌Toll样受体4mRNA及蛋白表达均明显降低,其TLR4/GAPDH比值分别为0.70和0.37。免疫组化研究结果显示,TLR4蛋白分布于心肌细胞,胞核未着色。 结论:随着机体老化,心肌TLR4表达降低,可能与老龄心肌对感染的易患性增加有关。 AIM: To investigate the age-related changes of Toll-like receptor 4(TLR4) expression, and to seek the method for prevention and cure of aging myocardium lesion. METHODS: Female adult(8 - 12 w, n = 5) and elder (20m, n = 5) BALB/c mice were studied, their TLR4 mRNA and protein expression were measured by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: Compared with adult mice, TLR4 expression in hearts of elder BALB/c mice decreased significantly, the ratios of TLR4/GAPDH were 0. 70 and 0. 37, respectively. The results of immunohistochemistry showed that TLR4 protein distributed in myocardial cells, and nucleus was not pig-menting. CONCLUSION: With the aging of the organ, the declining TLR4 expression may be related to the high susceptibility of infection in aging myocardium.
出处 《中国临床康复》 CSCD 2004年第9期1656-1657,共2页 Chinese Journal of Clinical Rehabilitation
基金 国家重点基础研究发展规划(973)部分赞助(G2000057004)~~
  • 相关文献

参考文献2

二级参考文献24

  • 1[1]Kumar A,Thota V,Dee L,et al.Tumor necrosis factor α and interleukin 1β are responsible for in vitro myocardial cell depression induced by human septic shock serum.J Exp Med 1996;183:949- 58
  • 2[2]Kapadia S,Lee J,Torre-Amione G,et al.Tumor Necrosis Factor α gene and protein expression in adult feline myocardium after endotoxin administration.J Clin Invest 1995;96:1042- 52
  • 3[3]Hoshino K,Takeuchi O,Kawai T,et al.Cutting edge: toll-like receptor 4(TLR4)-deficient mice are hyporesponsive to lipopolysaccharide:evidence for TLR4 as the Lps gene product.J Immunol 1999;162:3749- 52
  • 4[4]Yamamoto K,Shimokawa T,Yi H,et al.Aging accelerates endotoxin-induced thrombosis: increased responses of plasminogen activator inhibitor-1 and lipopolysaccharide signaling with aging.Am J Pathol 2002;161:1805- 14
  • 5[5]Renshaw M,Rockwell J,Engleman C,et al.Cutting edge: Impaired Toll-like receptor expression and function in aging.J Immunol 2002;169:4697- 701
  • 6[6]Knuefermann P,Nemoto S,Misra A,et al.CD14-deficient mice are protected against lipopolysaccharide-induced cardiac inflammation and left ventricular dysfunction.Circulation 2002;106:2608- 15
  • 7[7]Parker MM,Shelhamer JH,Bacharach SL,et al.Profound but reversible myocardial depression in patients with septic shock.Ann Intern Med 1984;100:483- 90
  • 8[8]Frantz S, Kobzik L,Kim YD,et al.Toll4 (TLR4) expression in cardiac myocytes in normal and failing myocardium.J Clin Invest 1999;104:271- 80
  • 9[9]Triantafilou M,Triantafilou K.Lipopolysaccharide recognition:CD14,TLRs and the LPS-activation cluster.Trends Immunol 2002; 23:301- 4
  • 10Varo-Thorbock R,Ruis-Rocpena E,Guerrero-Fernandes JA.Effects of human growth horrnono on the catabolic state after surgical trauma.Hourm Res 1996;45(1-2):55-60.

共引文献18

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部