论文部分内容阅读
目的探讨核因子-κB(NF-κB)信号途径在川崎病(KD)冠状动脉免疫损害中的作用。方法2004年10月至2005年12月武汉市儿童医院收治的KD患儿48例,将患儿分为两组:冠状动脉损害亚组(CALs亚组)11例,无冠状动脉损害亚组(Non-CALs亚组)37例。感染对照组:同年龄组感染发热住院患儿18例。健康对照组:同年龄组健康体检儿童12例。采用免疫印迹(Western blot)法检测外周血单个核细胞(PBMC)中NF-κBp65及IκBα蛋白表达;采用逆转录聚合酶链反应(RT-PCR)检测TNF-α、MCP-1mRNA表达。结果(1)KD组NF-κBp65明显高于两对照组[(16.53±4.81)vs.(8.37±3.15,0.33±0.05)(P<0.001)]。CALs亚组NF-κBp65显著高于Non-CALs亚组[(22.86±3.11)vs.(13.55±3.23)(P<0.05)]。KD组NF-κBp65抑制物IκBα明显低于感染对照组及健康对照组[(5.69±2.03)vs.(21.22±4.37,28.58±7.89)(P<0.001)]。CALs亚组中胞核NF-κBP65/IκBα比值与CALs的严重程度呈正相关(r=0.536,P<0.05)。(2)KD组TNF-αmRNA、MCP-1mRNA较两对照组明显升高[(7.02±2.91)vs.(3.05±2.33,0.61±0.38)(P<0.01);(3.89±1.10)vs.(1.11±0.42,0.04±0.01)(P<0.01)]CALs亚组TNF-αmRNA、MCP-1mRNA明显高于Non-CALs组[(8.79±1.52)vs.(6.13±2.52)(P<0.05);(4.26±0.78)vs.(3.01±0.53)(P<0.05)]。结论NF-κBp65信号通路的活化参与KD急性期血管炎的发生机制,可能参与冠状动脉损害的形成。
Objective To investigate the role of nuclear factor-kappa B (NF-κB) signaling pathway in coronary artery injury caused by Kawasaki disease (KD). Methods Forty-eight children with KD admitted to Wuhan Children’s Hospital from October 2004 to December 2005 were divided into two groups: 11 patients with coronary artery lesion subgroup (CALs subgroup) and no coronary artery lesion subgroup Non-CALs subgroup) 37 cases. Infection control group: In the same age group, 18 cases of fever hospitalized children. Healthy control group: 12 healthy children in the same age group. The expressions of NF-κBp65 and IκBα in peripheral blood mononuclear cells (PBMCs) were detected by Western blot. The mRNA expressions of TNF-α and MCP-1 were detected by reverse transcription-polymerase chain reaction (RT-PCR) Results (1) NF-κBp65 in KD group was significantly higher than that in two control groups [(16.53 ± 4.81) vs. (8.37 ± 3.15,0.33 ± 0.05)] (P <0.001). NF-κBp65 in CALs subgroup was significantly higher than that in Non-CALs subgroup (22.86 ± 3.11 vs. 13.55 ± 3.23, P <0.05). The IκBα of NF-κBp65 inhibitor in KD group was significantly lower than that in infection control group and healthy control group [(5.69 ± 2.03) vs. (21.22 ± 4.37, 28.58 ± 7.89) (P <0.001)]. The nuclear NF-κB P65 / IκBα ratio in CALs subgroup was positively correlated with the severity of CALs (r = 0.536, P <0.05). (2) The levels of TNF-αmRNA and MCP-1mRNA in KD group were significantly higher than those in control group [(7.02 ± 2.91) vs. (3.05 ± 2.33,0.61 ± 0.38, P <0.01; 3.89 ± 1.10 vs 1.11 ± 0.42,0.04 ± 0.01) (P <0.01). The levels of TNF-α mRNA and MCP-1 mRNA in CALs subgroup were significantly higher than those in Non-CALs group (8.79 ± 1.52 vs. 6.13 ± 2.52, P <0.05) (4.26 ± 0.78) vs. (3.01 ± 0.53) (P <0.05)]. Conclusion The activation of NF-κBp65 signaling pathway is involved in the pathogenesis of KD acute vasculitis and may be involved in the formation of coronary artery lesion.