Effect of curcumin on expression of SLPI,TNF-αand IL-1βin BEAS-2B cells induced by Streptococcus pneumoniae
10.3969/j.issn.1000-4718.2018.02.021
- VernacularTitle:姜黄素对肺炎链球菌诱导BEAS-2B细胞SLPI、TNF-α和IL-1β表达的影响
- Author:
Lu YU
1
;
Li LIN
;
Hai-Yan LI
;
Shun-Hang WEN
;
Hai-Lin ZHANG
;
Chang-Chong LI
Author Information
1. 温州医科大学附属第二医院
- Keywords:
Cucrcumin;
Streptococcus pneumoniae;
Secretory leukocyte protease inhibitor;
Toll-like receptor 2;
Nuclear factor-κB
- From:
Chinese Journal of Pathophysiology
2018;34(2):321-327
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To explore the effect of curcumin(Cur)and curcuminoids(Y20 and 6B)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-2B 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-αand IL-1βat 3 h,6 h and 9 h in control group,SP infection group,Cur treatment group,Y20 treatment group and 6B treatment group were measured by qPCR.The protein levels of TNF-αand IL-1βin 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 6B treatment groups compared with SP group(P<0.05).The protein levels of TLR2 and p-NF-κB p65 were sig-nificantly increased after SP stimulation.After treatment with Cur,Y20 and 6B,the protein levels of TLR2 and p-NF-κB p65 were significantly decreased(P<0.05).The levels of TNF-αand IL-1βwere significantly increased after SP stimula-tion.Cur,Y20 and 6B significantly decreased the levels of TNF-αand IL-1βin the supernatant(P<0.05).CONCLU-SION: Cur, Y20 and 6B increase SLPI expression, reduce the expression of inflammatory cytokines TNF-αand IL-1β. The possible mechanism might be associated with inhibiting TLR 2 expression and down-regulating the transcriptional activity of NF-κB.
