摘要
目的:探讨姜黄素(Cur)及其衍生物Y20和6B对肺炎链球菌(SP)诱导的BEAS-2B细胞分泌型白细胞蛋白酶抑制因子(SLPI)、肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)表达的调节及可能机制。方法:建立体外SP感染模型,采用q PCR检测对照组、感染组以及Cur、Y20和6B处理组在感染1、3、6和9 h SLPI及感染3、6和9 h TNF-α和IL-1β的mRNA水平,ELISA法检测TNF-α和IL-1β的蛋白分泌水平,Western blot实验检测各时点Toll样受体2(TLR2)和磷酸化核因子κB(NF-κB)p65的蛋白水平。结果:q PCR结果显示,Cur、Y20和6B药物处理组SLPI的mRNA表达较SP感染组增加(P<0.05),TNF-α和IL-1β的mRNA表达较SP感染组明显下降(P<0.05);ELISA结果显示,感染不同时点的TNF-α和IL-1β含量在药物处理组中均下降(P<0.05);Western blot结果显示,SP感染3、6和9 h在药物处理组中TLR2和p-NF-κB p65的蛋白水平较感染组下降(P<0.05)。结论:在不同感染时间,Cur、Y20和6B促进SP感染的BEAS-2B细胞SLPI表达,减少TNF-α和IL-1β分泌,其机制可能与抑制TLR2表达、下调NF-κB转录活性有关。
AIM: To explore the effect of curcumin( Cur) and curcuminoids( Y20 and 6 B) on the expression of secretory leukocyte protease inhibitor( SLPI),tumor necrosis factor-α( TNF-α) and interleukin-1β( IL-1β) induced by Streptococcus pneumoniae( SP) and the possible mechanism. METHODS: BEAS-2 B cells incubated with SP were set up as an inflammation model of pneumonia. The mRNA levels of SLPI at 1 h,3 h,6 h and 9 h,and the mRNA expression of TNF-α and IL-1β at 3 h,6 h and 9 h in control group,SP infection group,Cur treatment group,Y20 treatment group and 6 B treatment group were measured by q PCR. The protein levels of TNF-α and IL-1β in the culture supernatant were measured by ELISA. The protein levels of Toll-like receptor 2( TLR2) and phosphorylated nuclear factor-κB( p-NF-κB)p65 at 3 h,6 h and 9 h were determined by Western blot. RESULTS: The mRNA level of SLPI was increased in Cur,Y20 and 6 B treatment groups compared with SP group( P 〈 0. 05). The protein levels of TLR2 and p-NF-κB p65 were significantly increased after SP stimulation. After treatment with Cur,Y20 and 6 B,the protein levels of TLR2 and p-NF-κB p65 were significantly decreased( P 〈 0. 05). The levels of TNF-α and IL-1β were significantly increased after SP stimulation. Cur,Y20 and 6 B significantly decreased the levels of TNF-α and IL-1β in the supernatant( P 〈 0. 05). CONCLUSION: Cur,Y20 and 6 B increase SLPI expression,reduce the expression of inflammatory cytokines TNF-α and IL-1β.The possible mechanism might be associated with inhibiting TLR2 expression and down-regulating the transcriptional activity of NF-κB.
作者
余璐
林立
李海燕
温顺航
张海邻
李昌崇
YU Lu;LIN Li;LI Hai-yan;WEN Shun-hang;ZHANG Hai-lin;LI Chang-chong(The Second Affiliated Hospital and Yuying Children’s Hospital,Wenzhou Medical Universit)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2018年第2期321-327,共7页
Chinese Journal of Pathophysiology
基金
浙江省自然科学基金资助项目(No.LQ17H010003
No.LZ13H010001)
国家自然科学基金资助项目(No.81700011)
浙江省教育厅项目(No.Y201432837)
温州市科技局基金资助项目(No.Y20140668)
国家临床重点专科开放课题(No.20130209)