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周佾龙, 杨韶华, 张弛等. 长链非编码基因MALAT1对LPS诱导的脓毒症大鼠免疫反应的调节作用及机制[J]. koko体育app 学报（医学版）, 2018, 49(6): 865-870.
引用本文: 周佾龙, 杨韶华, 张弛等. 长链非编号表观遗传MALAT1对LPS引发的脓毒症大鼠抗体发生反应的调理帮助及制度化[J]. 安徽师范大学学报（医学界版）, 2018, 49(6): 865-870.
ZHOU Yi-long, YANG Shao-hua, ZHANG Chi. et al. LncRNA MALAT1 Modulates the Immunoreaction of Rats with Lipopolysaccharide-induced Sepsis by Targeting the miR-146a/NF-κB P65 Pathway[J]. Journal of Sichuan University (Medical Sciences), 2018, 49(6): 865-870.
Citation: ZHOU Yi-long, YANG Shao-hua, ZHANG Chi. et al. LncRNA MALAT1 Modulates the Immunoreaction of Rats with Lipopolysaccharide-induced Sepsis by Targeting the miR-146a/NF-κB P65 Pathway[J]. Journal of Sichuan University (Medical Sciences), 2018, 49(6): 865-870.

长链非编码基因MALAT1对LPS诱导的脓毒症大鼠免疫反应的调节作用及机制

LncRNA MALAT1 Modulates the Immunoreaction of Rats with Lipopolysaccharide-induced Sepsis by Targeting the miR-146a/NF-κB P65 Pathway

  • 摘要: 目的 探索长链非编码基因MALAT1对脂多糖(LPS)诱导的U937细胞和脓毒症大鼠体内免疫反应的调节作用及其分子机制。方法 将U937细胞分为6组：U937对照组，LPS组，scramble组，si-MALAT1组，miR-146a inhibitor组和si-MALAT1+miR-146a inhibitor组。将20只SD大鼠分为健康对照组，LPS模型组， scramble干预组和si-MALAT1干预组。运用实时定量PCR (qRT-PCR)检测各组U937细胞和大鼠肺组织中MALAT1与miR-146a的表达；荧光素酶报告分析确认MALAT1与miR-146a的靶向关系；Western blot检测p-P65，P65，TNF-α和iNOS表达；免疫组化检测肺组织TNF-α和iNOS表达情况。结果 在LPS组U937细胞中MALAT1相对表达量高于U937(P<0.01)。与scramble组相比，si-MALAT1组MALAT1相对表达量降低，miR-146a相对表达量升高(P<0.01)。MALAT1与miR-146a存在靶向关系。与LPS组相比， si-MALAT1组p-P65/P65的比值，TNF-α和iNOS的相对表达量降低；miR-146a inhibitor组p-P65/P65的比值，TNF-α和iNOS的相对表达量升高(P<0.01)。与miR-146a inhibitor组相比，si-MALAT1和miR-146a inhibitor共转染组p-P65/P65的比值，TNF-α和iNOS的相对表达量降低(P<0.01)。与健康对照组相比，LPS组和scramble组大鼠miR-146a相对表达量降低，p-P65/P65的比值升高(P<0.01)。与scramble组相比，si-MALAT1组大鼠miR-146a相对表达量升高，p-P65/P65的比值降低(P<0.01)。LPS组和scramble组大鼠中TNF-α和iNOS阳性细胞数目高于健康对照组(P<0.01)。与scramble组相比，si-MALAT1组大鼠中TNF-α和iNOS阳性细胞数目减少(P<0.01)。结论 MALAT1可靶向miR-146a/NF-κB P65对LPS诱导的脓毒症大鼠的免疫反应进行调节。  
    Abstract: Objective To determine the regulatory and molecular mechanism of lncRNA MALAT1 in response to sepsis induced by lipopolysaccharide (LPS) in rats. Methods The expressions of lncRNA MALAT1 and miR-146a in U937 cells and peripheral blood samples of the rats with and without LPS-induced sepsis were detected using quantitative real-time reverse transcription PCR (qRT-PCR). The relationship between lncRNA MALAT1 and miR-146a was affirmed through luciferase assay. The expressions of p-P65, P65, TNF-α and iNOS were tested by Western blot. The expressions of TNF-α and iNOS in the lung tissues of the rats were measured by immunohistochemistry. Results The rats with LPS-induced sepsis had higher expressions of lncRNA MALAT1 in U937 cells than those without sepsis (P<0.001). In comparison with scramble, si-MALAT1 attenuated the expression of lncRNA MALAT1 and increased the expression of miR-146a (P<0.001). MiR-146a was the target of lncRNA MALAT1. si-MALAT1 decreased the p-P65/P65 ratio and and the expressions of TNF-α and iNOS in the rats with LPS-induced sepsis. In contrast, miR-146a inhibitor increased p-P65/P65 ratio and the expressions of TNF-α and iNOS in the rats with LPS-induced septis (P<0.001). Co-transfection with si-MALAT1 attenuated the elevated level of p-P65/P65 ratio and expressions of TNF-α and iNOS resulting from miR-146a inhibitor (P<0.001). LPS and scramble decreased the expression of miR-146a and increased the p-P65/P65 ratio compared with the healthy controls (P<0.01). Compared with scramble, si-MALAT1 increased the expression of miR-146a and attenuated the p-P65/P65 ratio (P<0.01). Higher numbers of TNF-α and iNOS positive cells were found in those with LPS-induced sepsis and those with scramble interventions (P<0.001). Compared with scramble, si-MALAT1 reduced the number of TNF-α and iNOS positive cells (P<0.01). Conclusion LncRNA MALAT1 modulates the immunoreaction of rats with LPS -induced sepsis by targeting miR-146a/NF-κB P65.  
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