摘要
目的:研究奇士乐对卡介苗联合脂多糖所致免疫性肝损伤小鼠的影响。方法:采用BCG 2.5mg静脉注射致敏小鼠,d10给予LPS 7.5μg静脉攻击,复制小鼠免疫性肝损伤模型,连续给药10天。分光光度法测定血清NO,肝匀浆中MDA、SOD、iNOS含量;免疫组化技术观察肝脏NF-κBp65表达情况。结果:QSL能降低免疫性肝损伤小鼠血清中NO和肝匀浆中MDA、iNOS水平,升高其低下的SOD水平;同时降低NF-κBp65在肝脏中的表达。结论:QSL对免疫性肝损伤小鼠具有保护作用,其机制可能与减少自由基的产生,抑制脂质过氧化,调节NF-κB通路,减少炎症介质的释放有关。
Objective： To study effects of QSL on immunological liver injury in mice.Methods： The model of mouse immunological liver injury was induced by injection of BCG and lipopolysaccharide（LPS） from tail vein.The nitric oxide（NO） level in serum and alondiadehyde（MDA） content,superoxide dismutase（SOD） activities in liver homogenate were assayed by spectrophotometry.NF-κBp65 in hepatic tissues was determined by the method of immunohistochemistry.Results： Immunological liver injury was successfully induced by BCG ＋LPS.QSL could decrease NO level in serum and MDA, iNOS, NOS contents and prevented the reduction of SOD activity in liver homogenate. Meanwhile, QSL were found to inhibit the expression of NF-KBp65 in liver tissue. Conclusion： The results showed that QSL have significant protective action on mice immunological liver injury. Its mechanism might be related to depleting oxygen free radical, suppressing cell lipid peroxidation and accommodating the path of NF-κB , diminishing mediators of inflammation.
出处
《中药药理与临床》
CAS
CSCD
北大核心
2009年第4期60-62,共3页
Pharmacology and Clinics of Chinese Materia Medica
基金
国家科技部十五重大科技专项(863)资助项目(编号:2004AA2Z3322)
关键词
奇士乐
免疫性肝损伤
脂质过氧化
核因子-ΚB
Qishile
immunological liver injury
lipid peroxidation
nuclear factor kappa B
