CAJ | 학술논문

目的探讨补体C1q对Aβ纤维诱导的小胶质细胞炎性反应的影响. 方法在一定浓度Aβ纤维刺激的基础上,向BV-2小胶质细胞中加入不同浓度C1q,并且利用C1qA竞争性与Aβ的结合以完成对比实验,利用夹心酶联免疫吸附法(ELISA)测定上清液及细胞裂解液中白介素(IL)-6和肿瘤坏死因子(TNF)-α的浓度. 结果在Aβ纤维刺激下,加入50 nmoI/L补体C1q后,上清液TNF-α浓度较单独加入Aβ纤维明显增加(F=1177.270,P＜0.05)；但在此基础上加入补体C1qA后,TNF-α浓度降低(P＜0.05).除阳性对照组外,各实验组上清液及细胞裂解液中IL-6浓度相互比较差异无统计学意义(均P＞0.05). 结论补体C1q可能通过促炎性因子TNF-α增强了Aβ诱导的BV-2小胶质细胞的炎性反应.
목적 탐토보체C1q대Aβ섬유유도적소효질세포염성반응적영향. 방법 재일정농도Aβ섬유자격적기출상,향BV-2소효질세포중가입불동농도C1q,병차이용C1qA경쟁성여Aβ적결합이완성대비실험,이용협심매련면역흡부법(ELISA)측정상청액급세포렬해액중백개소(IL)-6화종류배사인자(TNF)-α적농도. 결과 재Aβ섬유자격하,가입50 nmoI/L보체C1q후,상청액TNF-α농도교단독가입Aβ섬유명현증가(F=1177.270,P＜0.05)；단재차기출상가입보체C1qA후,TNF-α농도강저(P＜0.05).제양성대조조외,각실험조상청액급세포렬해액중IL-6농도상호비교차이무통계학의의(균P＞0.05). 결론 보체C1q가능통과촉염성인자TNF-α증강료Aβ유도적BV-2소효질세포적염성반응.
Objective The impact of complement Clq on inflammation in beta amyloidstimulated microglia.Methods After the cultured BV-2 microglial cells were treated with 100mg/L beta-amyloid fibers (fAβs),some of them were given C1q,others wcrc given C1q and C1qA.Then,interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) in the supernatant and cell lysate were determined by the sandwich ELISA.Results A significant increase in TNF-α started at giving 50 nmol/L C1q after 100 mg/L fAβs (F =1177.27,P＜ 0.05),while the release of TNF-α was significantly suppressed by using 50 nmol/L C1qA on basis of this(P＜0.05).The level of IL-6 showed no above change.Conclusions C1q may enhance the inflammation of Aβ-induced BV-2 microglia cells and TNF-α may play important role in this effect.