知母皂苷对脂多糖诱导巨噬细胞炎症介质释放影响  

Effect of SAaB on LPS-induced release of inflammatory mediators in cultured macrophages

作　　者：刘卓[1] 隋海娟[1] 闫恩志[1] 刘婉珠[1] 金英[1] 

机构地区：[1]辽宁医学院药理学教研室,辽宁锦州121001

出　　处：《中国公共卫生》2013年第3期384-386,共3页Chinese Journal of Public Health

基　　金：辽宁省教育厅创新团队项目(LT2010064);辽宁省教育厅一般项目(L2011143);辽宁医学院院内资助课题(Y2010Z003)

摘　　要：目的观察知母皂苷是否能对抗脂多糖(LPS)引起的小鼠腹腔巨噬细胞炎症介质释放并探讨丝裂原活化蛋白激酶(MARK)信号转导通路影响。方法实验设对照组,脂多糖组,知母皂苷低、中、高剂量组和阻断剂组,Griess法测定巨噬细胞培养上清液一氧化氮(NO)含量变化;酶联免疫吸附法测定巨噬细胞培养上清液中白介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)含量;免疫化学染色法观察诱导型一氧化氮合酶(iNOS)表达。结果加入脂多糖作用2 h,巨噬细胞上清液中NO含量明显增加,24 h达高峰,知母皂苷(10、30、100μmol/L)可抑制脂多糖引起的IL-1β、TNF-α、NO增加和iNOS表达增多,100μmol/L知母皂苷组IL-1β、TNF-α和NO水平分别从(698.8±32.0)ng/L、(257.4±27.3)ng/L和(181.0±19.9)μmol/L下降到(382.7±48.9)ng/L、(111.6±23.9)ng/L和(82.6±18.1)μmol/L;SP600125和SB203580均可不同程度抑制脂多糖引起的巨噬细胞IL-1β、TNF-α和NO增加;S-甲基异硫脲可完全对抗脂多糖引起NO释放。结论知母皂苷明显抑制脂多糖引起的巨噬细胞炎症因子释放,其机制与下调p38MAPK和c-Jun氨基末端激酶(JNK)信号通路表达有关。Objective To investigate inhibitory effect and possible mitogen-activated protein kinase signaling mech- anism of saponin from Anemarrhena asphdeloids Bge （ SAaB ） on the release of inflammatory mediators induced by li- popolysaccharides（LPS） in cultured mouse peritoneal macrophages. Methods After stimulation with LPS, the superna- tants of macrophages were collected and analyzed for tumor necrosis factor-α（ TNF-α）, interleukin-1 β（ IL-1β）and nitric oxide （NO） generation, and protein expression of inducible nitric oxide synthase （ iNOS ） in macrophages was determined with immunocytochemical staining. Results LPS significantly inducedan increase in iNOS protein expression and the production of TNF-α, IL-1β, and NO in cultured macrophages. SAaB （100 μmol/L） significantly suppressed LPS-in- duced increase in iNOS protein level. In addition, SAaB （10,30 and 100 μmol/L） also decreased TNF-α, IL-1β and NO generation in supernatants of cultured macrophages, with the decreases of TNF-α,IL-1β,and NO from 698. 8 ±32. 0 ng/L, 257.4±27.3 ng/L,and 181.0±19.9 p, mol/L to 382. 7± 48.9 rig/L, 111.6 ± 23.9 ng/L, and 82. 6 ±18. 1 μmol/L, respectively. SB203580 and SP600125 could distinctly inhibit the production of TNF-α, IL-1β, NO, and the expression of iNOS. Conclusion SAaB could significantly inhibit the over-release of inflammatory mediators induced by LPS in cul- tured mouse peritoneal macrophages, which may be related to the downregulation of mitogen-activated protein kinase （MARK） signal transduction pathway.

关 键 词：知母皂苷 巨噬细胞 脂多糖 炎症介质 丝裂原活化蛋白激酶(MARK) 

分 类 号：R972.6[医药卫生—药品]