摘要
目的探讨前胡甲素(Pd-Ia)对脂多糖(lipopolysaccha-ride,LPS)诱导的内皮细胞中细胞因子表达的影响及其作用机制。方法体外培养人脐静脉内皮细胞(HUVECs),用1mg·L-1LPS和不同浓度的Pd-Ia(10,20,40μmol·L-1)孵育24 h,采用荧光实时定量PCR检测TNF-α、IL-1β、PPARs(过氧化物酶体增殖激活受体)的表达。进一步在HUVECs中采用siRNA干扰PPARα后观察Pd-Ia的抗炎效应的变化。结果①Pd-Ia可以抑制LPS诱导的内皮细胞中TNF-α、IL-1β的表达。②Pd-Ia选择性上调LPS诱导的内皮细胞中PPAR-α的表达,而对PPAR-β、PPAR-γ的表达没有影响。③采用了siRNA特异性沉默PPARα后,Pd-Ia对TNF-α、IL-1β的下调作用被一定程度的逆转。结论 Pd-Ia对LPS诱导的内皮炎症反应有抑制作用,其机制与激活PPARα有关。
Aim To investigate the effect of Pd-Ia on the expression of cytokines in LPS-induced HUVECs and its mechanisms.Methods HUVECs were treated with 1 mg·L-1 LPS and different concentrations of Pd-Ia（10,20,40 μmol·L-1） for 24h,the expression of TNF-α,IL-1β,PPARα,PPARβ,PPARγ was detected by Real-time PCR.To investigate the mechanism of the anti-inflammation of Pd-Ia,siRNA was added to knockdown PPARα.Results Pd-Ia down-regulated TNF-α,IL-1β mRNA expression and selectively up-regulated PPARα,but it had no effect on PPARβ and PPARγ mRNA expression in LPS-activated HUVECs.PPARα knockdown could attenuate the anti-inflammatory effect of Pd-Ia.Conclusions Pd-Ia inhibits the inflammatory response of endothelial cells to the stimulation of LPS,which is related to the activation of PPARα.It suggests that Pd-Ia exerts potential anti-inflammatory effect on the modulation of various inflammatory processes such as atherosclerosis.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2012年第11期1594-1597,共4页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No 81270294)
福建省科技计划重点项目(No 2010Y0053)
福建省自然科学基金资助项目(No 2012J01415)
