中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2008年
12期
878-882
,共5页
吴升华%廖培元%张永梅%董玲
吳升華%廖培元%張永梅%董玲
오승화%료배원%장영매%동령
脂氧素类%白三烯B4%脂氧合酶%儿童%急性链球菌感染后肾炎
脂氧素類%白三烯B4%脂氧閤酶%兒童%急性鏈毬菌感染後腎炎
지양소류%백삼희B4%지양합매%인동%급성련구균감염후신염
Lipoxins%Leukotriene B4%Lipoxygenase%Children%Acute poststreptococcal glomerulonephritis
目的 探讨急性链球菌感染后肾炎(APSGN)患儿血、尿脂氧素A4(LXA4)、白三烯B4(LTB4)和白细胞15-脂氧化酶(15-LO)水平变化的意义.方法 分别在22例APSGN患儿发病≤3 d(急性期)、10～14 d(恢复早期)和6～8周(恢复晚期)留取标本,采用ELISA方法测定血、尿LXA4和LTB4.对8例患儿应用RT-PCR方法测定白细胞15-LO表达.体外趋化法测定白细胞LTB4和中性粒细胞趋化功能.对照组为健康体检儿童.结果 患儿急性期的血、尿LXA4和白细胞15-LO表达升高,恢复早期进一步升高(均P＜0.01);在恢复晚期有所降低,但仍高于健康儿童(均P＜0.01).患儿急性期的血、尿LTB4高于健康儿童(P＜0.01),在恢复早期和恢复晚期逐渐降低,仍高于健康儿童(P＜0.01).体外应用15-S-羟二十碳四烯酸(15-S-HETE)或LXA4可抑制患儿白细胞合成LTB4,抑制中性粒细胞趋化功能.结论 患儿血、尿LXA4和白细胞15-LO表达在恢复早期与血、尿LTB4变化相反.15-S-HETE和LXA4通过抑制LTB4而发挥抗炎作用,促进APSGN疾病的恢复.
目的 探討急性鏈毬菌感染後腎炎(APSGN)患兒血、尿脂氧素A4(LXA4)、白三烯B4(LTB4)和白細胞15-脂氧化酶(15-LO)水平變化的意義.方法 分彆在22例APSGN患兒髮病≤3 d(急性期)、10～14 d(恢複早期)和6～8週(恢複晚期)留取標本,採用ELISA方法測定血、尿LXA4和LTB4.對8例患兒應用RT-PCR方法測定白細胞15-LO錶達.體外趨化法測定白細胞LTB4和中性粒細胞趨化功能.對照組為健康體檢兒童.結果 患兒急性期的血、尿LXA4和白細胞15-LO錶達升高,恢複早期進一步升高(均P＜0.01);在恢複晚期有所降低,但仍高于健康兒童(均P＜0.01).患兒急性期的血、尿LTB4高于健康兒童(P＜0.01),在恢複早期和恢複晚期逐漸降低,仍高于健康兒童(P＜0.01).體外應用15-S-羥二十碳四烯痠(15-S-HETE)或LXA4可抑製患兒白細胞閤成LTB4,抑製中性粒細胞趨化功能.結論 患兒血、尿LXA4和白細胞15-LO錶達在恢複早期與血、尿LTB4變化相反.15-S-HETE和LXA4通過抑製LTB4而髮揮抗炎作用,促進APSGN疾病的恢複.
목적 탐토급성련구균감염후신염(APSGN)환인혈、뇨지양소A4(LXA4)、백삼희B4(LTB4)화백세포15-지양화매(15-LO)수평변화적의의.방법 분별재22례APSGN환인발병≤3 d(급성기)、10～14 d(회복조기)화6～8주(회복만기)류취표본,채용ELISA방법측정혈、뇨LXA4화LTB4.대8례환인응용RT-PCR방법측정백세포15-LO표체.체외추화법측정백세포LTB4화중성립세포추화공능.대조조위건강체검인동.결과 환인급성기적혈、뇨LXA4화백세포15-LO표체승고,회복조기진일보승고(균P＜0.01);재회복만기유소강저,단잉고우건강인동(균P＜0.01).환인급성기적혈、뇨LTB4고우건강인동(P＜0.01),재회복조기화회복만기축점강저,잉고우건강인동(P＜0.01).체외응용15-S-간이십탄사희산(15-S-HETE)혹LXA4가억제환인백세포합성LTB4,억제중성립세포추화공능.결론 환인혈、뇨LXA4화백세포15-LO표체재회복조기여혈、뇨LTB4변화상반.15-S-HETE화LXA4통과억제LTB4이발휘항염작용,촉진APSGN질병적회복.
Objective To investigate the change of lipoxin A4 (LXA4), leuotriene B4(LTB4) in blood and urine and leukocyte 15-lipoxygenase (15-LO) of the children with acute poststreptococcal glomendonephritis (APSGN) and to evaluate its significance. Methods Blood and urinary levels of LXA4 and LTB4 were measured with ELISA within 3 days (acute phase), 10 to 14 days (early resolution phase) and 6 to 8 weeks (late resolution phase) respectively after onset of APSGN in 22 patients. In 8 children with APSGN, expression level of leukocyte 15-LO mRNA was examined with RT-PCR. Leukocyte LTB4 synthesis was assessed with ELISA. Chemotactic effect of LTB4, LXA4 and 15-S-hydroxyeicosatetraenoic acid (15-S-HETE) on neutrophils was determined by in vitro chemotaxis assay. Twenty-two healthy children were served as control. Results Blood and urinary levels of LXA4 and leukocyte 15-LO mRNA were up-regnlated in acute phase, further increased in early resolution phase, and decreased in late resolution phase of APSGN, which were stir higher than those in the controls (P＜0.01). Blood and urinary levels of LTB4 were increased in acute phase (P＜0.01) and then were decreased in early resolution phase and hte resolution phase of APSGN, which were still higher than those in the controls (P＜0.01). Administration of 15-S-HETE or LXA4 in vitro inhibited LTB4-induced chemotactic effect on neutrophils of the patients,and inhibited the production of leukocyte LTB4. Conclusions Changes of blood and urinary levels of LXA4 and LTB4 in early resolution phase of APSGN are contrary. 15-S-HETE and LXA4may play a role in anti-inflammation and resolution of APSGN via inhibiting LTB4.
