摘要
目的 :旨在制造出接近临床病毒性肝炎发病机制的肝损伤动物模型。方法 :用不同数量的卡介苗 (BCG)及不同剂量的脂多糖 (LPS)诱导SD大鼠建立急性免疫性肝损伤模型 ,以大鼠血清转氨酶水平变化和肝脏病理学检查等指标作为肝损伤判断标准 ,并以流式细胞仪对该模型的血清CD3+ 、CD4 + 、CD8+ 细胞百分比计数 ,以ELISA法对TNFα -IgG、白介素 (IL - 6和IL -10 )水平进行了检测。结果 :“BCG +LPS”所造免疫性急性肝损伤模型当以BCG用量 5× 10 7个活菌 /只及LPS用量 30 μg·kg 1时ALT升高明显。肝脏组织病理损伤中“Ⅲ”级和“Ⅳ”级大于 70 %。其细胞因子水平较正常大鼠升高。对血清CD3+ 、CD4 + 、CD8+ 细胞百分比也有影响。结论 :以“BCG +LPS”所造模型比较成功 ,该模型能充分造成大鼠急性肝损伤 ,且能影响免疫系统 ,与病毒性肝炎的发病机制有较大相似 。
Objective:To produce liver injury model of animals to approach the pathogenesis of clinical viral hepatitis, and to advance investigation about fulminant viral hepatitis. [WT5HZ]Methods: Different doses of BCG and LPS were injected intraperitoneally (ip) to rats in which might induce acute immune liver injury . Hepatic injury were assessed by the level of serum transaminase and pathological changes of liver. The percentage of CD3 +、CD4 +and CD8 + cell was determined by flow cytometer in serum. Level of cytokines including tumor necrosis factor (TNFα), IL-6 and IL-10 in sera was detected by ELISA as well. [WT5HZ] Results:It is suitable that GPT and GOT were stepped up clearly when viable BCG 5×10 7 bacilli/rat/once,ip injection,10 days before assay and LPS 30 micrograms/kg body wt/once, ip injection,8 hr before the assay were used for establishing immunity acute liver injury model of rats. Grade Ⅲ(extensive liver cellular necrosis with hemorrhage, about 1/3-2/3, inflammation dip like sheet shape) and grade Ⅳ(extensive liver cellular necrosis with hemorrhage, above 2/3, mass inflammation dip) were more than 70% in liver pathological classify. Tite of CD8 +, CD3 +and CD4 + in rats serum might also be affected by this dose. [WT5HZ]Conclusion:BCG+PLS might induce acute liver injury model of rats successfully. It seemed to approach the pathogenesis of clinical viral hepatitis to an effect to immune system. [WT5HZ]
出处
《西北国防医学杂志》
CAS
2004年第5期345-347,共3页
Medical Journal of National Defending Forces in Northwest China
