摘要
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 This study aimed at investigating whether nuclear factor-kappa B （ NF-κB）, its inhibitor IκBα and it＇s regulations were involved in coronary artery lesions in the children with KD. Methods Based on color Doppler examination results,48 affected children in the KD group were divided into two groups： 11 cases in Coronary artery lesions group （CALs subgroup） and 37 cases in non-coronary artery lesions group （Non-CALs subgroup）. Infection control group： 18 cases of hospitalized infected children with fever of the same age. Healthy control group： 12 cases of healthy children of the same age visiting the hospital for physical examination. Western blot was used to detect the expression of NF-κBp65 and IκBα proteins in peripheral blood monouclear cells （ PBMC ） ; reverse transcription polymerase chain reaction （ RT-PCR ） was used to detect the expression of TNF-α and MCP-1 mRNA. Results （ 1 ） The value of NF-κBp65 （ optical density） in the PBMC in the KD group was significantly higher than that in the two control groups[ （ 16. 53 ± 4. 81 ） vs. （8. 37 ±3.15,0. 33 ±0. 05 ） （ P 〈 0. 001 ） ]. The value of NF-κBp65 in the CALs subgroup was significantly higher than that in the Non-CALs subgroup[ （ 22. 86 ± 3. 11 ） vs. （ 13.55 ± 3.23 ） （ P 〈 0. 05 ）]. The value of IκBα in the KD group was significantly lower than that in the infection control group and the healthy control group[ （ 5.69 ± 2.03 ） vs. （21.22±4.37,28.58 ±7.89） （ P 〈0.001） ]. （2） The value of TNF-α mRNA and MCP-1 mRNA （ O. D ratio） in the KD group were significantly higher than those in the two control groups[ （ 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 ） ], and those in the CALs subgroup was significantly higher than that in the Non-CALs subgroup [ （ 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 signal passage participates in the pathogenesis of vaseulitis of KD in acute stage, and may aggravate the vaseulitis of KD and plays a part in the formation of CALs.
出处
《中国实用儿科杂志》
CSCD
北大核心
2008年第6期433-435,共3页
Chinese Journal of Practical Pediatrics
基金
武汉市卫生局重点项目基金(WW200312052)资助
