Inhibition function of azithromycin on inflammation in HaCaT keratinocyte cell induced by interleukin-22
10.13699/j.cnki.1001-6821.2016.08.008
- VernacularTitle:阿奇霉素对白细胞介素－22诱导的 HaCaT角质形成细胞炎症干预作用
- Author:
Qing-Ning CHEN
1
;
Xiao-Chuan WANG
;
Peng DU
;
Mei JIN
;
Chu-Ming FAN
Author Information
1. 云南省第一人民医院 皮肤科
- Keywords:
azithromycin;
interleukin-22;
HaCaT keratinocyte cell;
cell inflammation
- From:
The Chinese Journal of Clinical Pharmacology
2016;32(8):696-699
- CountryChina
- Language:Chinese
-
Abstract:
Objectives To explore the inhibition function of azithromycin on inflammation function in HaCaT keratinocyte cell induced by interleukin-22 (IL-22).Methods The cases were randomly divided into normal group, model group (100 μg? mL-1 IL-22) , azithromycin low, medi-um and high dose groups (100, 300, 1000 μg? mL-1 ).The content of nitric oxide ( NO) in medium was determined by Gries method.The con-tent of tumor nuclear factor ( TNF-α) , IL-6, IL-6 was examed by enzyme linked immunosorbent assay ( ELISA) .The phosphorylation of nuclear factor kappa B ( NF-κB) p65 and the expression of inducible nitric oxide synthase ( iNOS ) was assayed by Western blot.The expre-ssion of NF-κB p65,iNOS,TNF-α,IL-6,IL-8 mRNA was assayed by reverse transcription polymerase chain reaction ( RT -PCR ) . Results Compared with model group, the concentration of NO, the expression of TNF-α, IL-6 , IL-8 protein and mRNA was lower than in three dose azithromycin groups ( P <0.05 ) . The expression of TNF-α, IL-6 protein in model group and azithromycin medium group were [(39.12 ±3.45) vs (16.37 ±1.28)], [( 30.42 ±2.97) vs (13.29 ±1.52)].The expression of TNF-α, IL-6 mRNA in model group and azithromycin medium group was [(1.28 ±0.11) vs (0.72 ±0.07)],[( 0.89 ±0.08) vs (0.53 ±0.04)].The expression of iNOS protein and mRNA, the phosphorylation of NF-κB p65 and the expression of NF-κB p65 mRNA was lower than in azithromycin medium and high dose groups ( P <0.05 ) . Conclusion The azithromycin could inhibit inflammation in HaCaT keratinocyte cell induced by IL -22, may be correlated with via blocking NF -κB signal pathway and down-regulation expression of iNOS.
