摘要
目的：观察肾小球炎症时浸润的巨噬细胞（GMO）产生白细胞介素-1（IL－1）以及细胞信号传递抑制剂Lisofyllline(LSF）的阻断作用。方法：采用加速型抗基底膜肾炎模型，分离提取肾炎鼠肾小球巨噬细胞（GMr），腹腔Md（P－M）及正常鼠腹腔M(N－PM）作为对照，胸腺细胞增殖法固定MIL－l的活性，Northe杂交检测MIL－1βmR－NA的表达。结果：GM在脂多糖（LPS)G刺激后其IL-1活性显著高于N－IM和P－M的L-1活性（P＜0．01）；LSF可抑制GMIL-1的活性，呈剂量依赖性（15tmol/L时P＜0．01，25mol/L时P＜O．01）；GMIL-1βmRNA的表达高峰在6h，12h，24h渐下降，各时间点均高于P-M.ISF在各时间点均可抑制GMIL－1βmRNA的表达。结论：肾小球肾炎对肾小球内浸润的M在炎症状态下处于激活状态，产生IL－1，加剧炎症反应；LSF可从转录水平上抑制GMIL－1的表达，为临床防治肾小球肾炎提供了新的途径。
To observe IL-1 production of glomerular M(GM@) derived from glomerulonephritis model and in-verstigate the effect of LSF (1 mol/L, 5mol/L,15mol/L, 25 mol/L), an inhibitor of phosphatidic acid,which blockpartial cell signal transduction pathways,on the IL-1 production of GM METHODS: Rat model of accelerated unti-basement membrane glomerulonephritis was adopted,GMd were isolated using a sterile sieving techniuqe. Own peritonealM of model rats (PM) and normal peritoneal Md (N-PM) were also obtained as control IL-1 activity was dethetedby thymocyte proliferation.IL-1 mRNA was detected by Northem blot. RESULTS: IL-1 activity of the supematant ofGM were significantly higher than that of the N - PM and P - M s(P < 0. 01). Pretreatment with LSF,IL-1 activ-ity of GM were lower and showed dose dependent (15 mol/L, P < 0. 01; 25 mol/L, P < 0.01). IL-1 mRNA expres-sion of GM were higher than that of P-M, LSF can inhibit the IL-1 mRNA expression of GM. ONCLUSION: LSFcan inhibit the overachvity of infiltrated GM in producing IL-1, and may be of use for clinical intervention in glomeru-lonephritis.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第10期948-950,共3页
Chinese Journal of Pathophysiology
