Recombinant human CC16 inhibits senescence in human bronchial epithelial cells induced by cigarette smoke extract
10.16016/j.2097-0927.202309135
- VernacularTitle:重组CC16蛋白质抑制香烟烟雾提取物诱导人支气管上皮细胞衰老的初步研究
- Author:
Ting LI
1
;
Xiaoxue YANG
;
Rui GAO
;
Xinyang LI
;
Hailong WANG
;
Min PANG
Author Information
1. 030001 太原,山西医科大学第一医院呼吸与危重症医学科,呼吸疾病防治与基础研究山西省重点实验室
- Keywords:
cellular senescence;
cigarette smoke extract;
CC16 protein;
P38 MAPK/ERK1/2
- From:
Journal of Army Medical University
2024;46(12):1410-1416
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect and mechanism of recombinant human CC16 protein(rhCC16)on cigarette smoke extract(CSE)-induced senescence of human bronchial epithelial cells(HBECs).Methods CCK-8 assay was used to evaluate the cell viability in HBECs after treated with 0％,1％,2.5％,5％,7.5％and 10％CSE and/or 0,10,100,250 and 500 ng/mL rhCC16.β-galactosidase staining was used to observe the activity of the enzyme in control,CSE,and CSE+rhCC16 treated HBECs.The mRNA levels of P16 and P21 in above cell groups were detected by real-time fluorescence quantitative PCR(qPCR),and the protein levels of P16,P21,p-P53,P38,p-P38,ERK1/2 and p-ERK1/2 were detected with Western blot in control group,CSE and CSE+rhCC16 groups.Results Compared with the control group,5％CSE stimulation for 72 h or the treatment of 500 ng/mL or lower dose of rhCC16 had no significant effect on cell viability of HBECs.Stimulation 5％CSE for 72 h resulted in significantly higher positive rate to β-galactosidase staining(P＜0.05),elevated mRNA and protein levels of P16 and P21(P＜0.05),and enhanced protein levels of p-P53,p-P38 and p-ERK1/2(P＜0.05)when compared with the control group.Compared with the simple CSE stimulation,250 ng/mL 1hCC16 treatment decreased positive rate to β-galactosidase staining(P＜0.05),reduced mRNA and protein levels of P16 and P21(P＜0.05)and protein levels of p-P53,p-P38 and p-ERK1/2(P＜0.05).Conclusion rhCC16 inhibits CSE-induced cellular senescence of HBECs,which may due to its suppression in P38 MAPK and ERK1/2 signaling pathway.
