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内毒素受体Tlr4及CD14基因在脓毒症大鼠肺、肝组织中的表达及其意义 被引量:10

Implication of Tlr4 and CD14 mRNA expression in lung and hepatic tissues in sepsis rats
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摘要 目的采用盲肠结扎穿孔(CLP)法制备脓毒症模型,探讨脓毒症时大鼠肺、肝组织内毒素受体Tlr4及CD14mRNA的改变及其意义。方法50只SD大鼠,随机分为正常对照组(10只)、CLP组(40只),CLP后24、48、72和96h处死动物,留取肺、肝、肾及空肠组织,分别检测Tlr4、CD14mRNA的表达。CLP组24、48、72和96h肺、肝组织Tlr4及CD14mRNA的表达升高,与对照组比较差异有统计学意义(P<0.05),而肾、空肠组织Tlr4及CD14mRNA的表达与对照组比较差异无统计学意义(P>0.05)。结论提示肺、肝组织中Tlr4及CD14基因的表达改变与脓毒症的发生发展过程有密切的关系。 Objective To investigate the expression of Tlr4 and CD14 mRNA in the lung and hepatic tissues in sepsis rats. Methods The sepsis model was made by cecal ligation and puncture(CLP). Fifty male SD rats were randomly divided into 5 groups: normal control (n = 10), CLP (subdivided into 24, 48,72,96 h post-CLP, n = 10 in each). At serial time points in each group, animals were sacrificed, and the tissues of lung, liver,, kidney and intestine were harvested to detect the expression of Tlr4 and CD14 mRNA by using reverse transcription polymerase chain reaction (RT-PCR). Results The expression levels of Tlr4 and CD14 mRNA were significantly increased in lung and hepatic tissues during 24-96 h after CLP as compared with control group (P〈 0.05), while in kidney and intestine there was no statistically significant difference (P 〉 0.05). Conclusion Tlr4 and CD14 may be a key factor in the development of excessive inflammatory response.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2005年第8期952-953,共2页 Chinese Journal of Experimental Surgery
关键词 内毒素受体 T1r4 CD14 基因表达 脓毒症 大鼠 肺组织 肝组织 Sepsis Toll like receptor Lipopolysaccharide
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参考文献4

  • 1Baker CC, Chaudry IH, Gaines HO, et al. Evaluation of factors affecting mortality rate after sepsis in a murine cecal ligation and puncture model. Surg, 1983, 94:331-335.
  • 2Hoffmann JA, Kafatos FC, Janeway CA, et al. Phylogenetic perspectives in innate immunity. Science, 1999, 284:1313-1317.
  • 3Hsu LC, Park JM, Zhang K, et al. The protein kinase PKR is required for macrophage apoptosis after activation of Toll-like receptor 4. Nature, 2004,428 : 341-345.
  • 4Miyake K. Innate recognition of lipopolysaccharide by Toll-like receptor 4-MD-2. Trends Microbiol, 2004, 12:186-192.

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