摘要
目的 观察山莨菪碱 (6 5 4 2 )和脂多糖 (LPS)共同处理单核细胞 (M )后对核因子 κB抑制蛋白(IκB)降解和核因子 κB(NF κB)活化的影响。方法 分离、培养M ,分为正常对照组 ;LPS刺激组 (LPS 10 μg/ml) ;6 5 4 2干预组 (6 5 4 2 10ng/ml预孵育 1h后加入LPS 10 μg/ml)。分别在刺激前 (0 )、刺激后 0 .2 5、0 .5、1和2h ,留取M。检测M中IκBα水平和核提取物中NF κB的活性。结果 LPS刺激组IκBα水平 15min开始降低 ,30min降到最低值 ;NF κB活性峰值显著高于刺激前和正常对照组 (P <0 .0 1)。 6 5 4 2干预后 ,IκBα水平最低值 ,显著高于LPS组 (P <0 .0 1)而NF κB活性虽较刺激前和正常对照组升高 ,但显著低于LPS组 (P <0 .0 1)。结论 LPS可诱导M的IκBα降解和NF κB激活 ,而 6 5 4 2能减少IκBα降解 ,抑制NF κB的活化。提示6 5 4
Objective To study the effects of ansodamine (654 2) and Lipopolysaccharide (LPS) on the level of IκB and activation of nuclear factor κB(NF κB) in monocytes. Methods Monocytes collected from volenteers were cultured and divided into 3 groups. Group 1 was the normal control, group 2 consisted of monocytes stimulated with 10 μg/ml LPS and group 3 in which the monocytes were pretreated with 10 ng/ml ansodamine and stimulated with 10 μg/ml LPS. The level of IκB and the activity of NF κB in the nuclear extract of the monocytes were examined before, 0.25, 0.5, 1 and 2 h after LPS stimulation. Results In group 2, the level of IκB began to decrease 0.25 h after LPS stimulation and reached the lowest point 0.5 h after. The peak activity of NF κB was significantly higher than the pre stimulational level and the level of the normal control ( P <0.01). In group 3 with the pretreatment of ansodamine, the lowest level of IκB remained significantly higher than that of group 2 ( P <0.01) and the activity of NF κB was higher than that of the normal control but significantly lower than the activity of group 2 ( P < 0.01). Conclusion LPS can induce the degradation of IκB protein and the activation of NF κB and ansodamine reduces the degradation of IκB protein and inhibits the activation of NF κB. These facts suggest that ansodamine exerts therapeutic and protective effects on the human body against the challenge of inflammation reaction syndrome and acute lung injury.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
2000年第6期545-548,共4页
Journal of Third Military Medical University
基金
国家自然科学基金重点资助项目!(39730210)
关键词
核因子k-B
山莨菪碱
急性肺损伤
全身炎症反应
nuclear factor kappa B inhibiting protein
nuclear factor kappa B
ansodamine
acute lung injury
