CAJ | 학술논문

目的：探讨核转录因子-κβ、白介素-8和肿瘤坏死因子-α在过敏性紫癜患儿中的表达及临床意义。方法选取2013年1月-2013年8月初次在我科住院并确诊为HSP的患儿为病例组(40例)，并选取同时期我院门诊体检的健康儿童20例为正常对照组，采用ELISA法检测各组患儿外周血单个核细胞NF-κβ活性及血清IL-8、TNF-α的表达水平。结果（1）病例组患儿外周血单个核细胞的NF-κβ活性明显高于正常对照组（P＜0.05)，且HSPN组外周血单个核细胞NF-κβ活性明显高于无肾损害HSP组（P＜0.05）；（2）病例组患儿血清IL-8、TNF-α水平明显高于正常对照组（P＜0.05），且HSPN组血清IL-8、TNF-α水平明显高于无肾损害HSP组（P＜0.05）；（3）无肾损害HSP组、HSPN组PBMC中NF-κβ活性分别与血清IL-8呈正相关（P＜0.05）、与血清TNF-α亦呈正相关（P＜0.05）。结论 NF-κβ、IL-8及TNF-α均参与了过敏性紫癜的发病过程。
목적：탐토핵전록인자-κβ、백개소-8화종류배사인자-α재과민성자전환인중적표체급림상의의。방법선취2013년1월-2013년8월초차재아과주원병학진위HSP적환인위병례조(40례)，병선취동시기아원문진체검적건강인동20례위정상대조조，채용ELISA법검측각조환인외주혈단개핵세포NF-κβ활성급혈청IL-8、TNF-α적표체수평。결과（1）병례조환인외주혈단개핵세포적NF-κβ활성명현고우정상대조조（P＜0.05)，차HSPN조외주혈단개핵세포NF-κβ활성명현고우무신손해HSP조（P＜0.05）；（2）병례조환인혈청IL-8、TNF-α수평명현고우정상대조조（P＜0.05），차HSPN조혈청IL-8、TNF-α수평명현고우무신손해HSP조（P＜0.05）；（3）무신손해HSP조、HSPN조PBMC중NF-κβ활성분별여혈청IL-8정정상관（P＜0.05）、여혈청TNF-α역정정상관（P＜0.05）。결론 NF-κβ、IL-8급TNF-α균삼여료과민성자전적발병과정。
Objective To investigate the changes of NF-κβin Peripheral Blood Mononuclear Cells and serum levels of IL-8, TNF-α,and probe their clinical significance in children with Henoch Schonlein purpura. Methods Forty children with HSP ad-mitted to our hospital in January 2013 to August 2013 and 20 healthy children enrolled in this study,served as case group and control group,respectively. The activation of NF-κβin Peripheral Blood Mononuclear Cells (PBMC) and the serum levels of IL-8,TNF-αwere detected by ELISA. Results (1)The activation of PBMC NF-κβin case group was significantly higher than that of normal control group (P<0.05),and the NF-κβactivity in no renal damage HSP group was significantly higher than that of the HSPN group (P<0.05);(2)The serum levels of IL-8 and TNF-αin case group was significantly higher than that of normal control group (P<0.05),and the serum levels of IL-8 and TNF-αin no renal damage HSP group were significantly higher than the HSPN group (P<0.05);(3)The activation of NF-κβwas positively correlated to the serum levels of IL-8 and TNF-αin no renal damage HSP group and HSPN group,respectively (P<0.05). Conclusion NF-κβ,IL-8 and TNF-α were involved in the pathogenesis of Henoch Schonlein purpura.