Effects of curcumin on the inflammatory reaction induced by LPS and the expression of SIGIRR in alveolar epithelial cells
10.3969/j.issn.1006-5725.2017.07.014
- VernacularTitle:姜黄素对脂多糖诱导肺泡上皮细胞炎性反应及单免疫球蛋白白介素-1相关蛋白表达的影响
- Author:
Huinan SUN
;
Xuxin CHEN
;
Zhihai HAN
- Keywords:
Curcumin;
Lipopolysacharride;
Alveolar epithelial cell;
Inflammation;
Single immunoglobin IL-1 receptor related protein
- From:
The Journal of Practical Medicine
2017;33(7):1070-1073
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of curcumine on the inflammation and expression of single immunoglobin IL-1 receptor related protein in alveolar epithelial cells induced by lipopolysacharride (LPS).Methods The rat type Ⅱ alveolar epithelial cells were cultured in vitro,and cell activity was measured when stimulated with LPS and different doses of curcumin.The level of tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in supematant was detected.Cells pretreated with curcumin (20 μmol/L),were stimulated with LPS (10 μg/mL).The nuclear protein and membrane protein was extracted to detect the expression level of nuclear transcription factor kappa B (NF-κB) and single immunoglobin IL-1 receptor related protein (SIGIRR).Results The cells activities were not affected by curcumin (5 ~30 pμmol/L) and LPS (10 μg/mL) (P < 0.05).Curcumin (5 ~30 μ mol/L) significantly inhibited LPS-induced overpression of TNF-α and IL-6 (P < 0.05).In 20 μ mol/L and 30 μ mol/L pretreatment groups,the inhibition of curcumin was most obvious,and there were no significant differences between the two groups (P < 0.05).Curcumin (20 μ mol/L) significantly inhibited the expression level of phosphorylation of NF-κB p65 in cell nucleus,while up-regulated the expression of SIGIRR (P < 0.05).Conclusion Curcumin inhibits the expression of inflammatory factor such as TNF-α and IL-6 as well as activation of NF-κB in alveolar epithelial cells induced by LPS.Up-regulating the expression level of negative regulatory molecules SIGIRR is one of the possible mechanism.