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

李婷; 杨晓雪; 高睿; 栗馨洋; 王海龙; 庞敏

doi:10.16016/j.2097-0927.202309135

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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

基础医学 | 更新时间：2026-01-09

- 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
- Recombinant human CC16 inhibits senescence in human bronchial epithelial cells induced by cigarette smoke extract
- 陆军军医大学学报 2024年46卷第12期页码：1410-1416
- 作者机构：
  
  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
  2.030600 山西晋中，山西医科大学基础医学研究中心
- 作者简介：
  
  [庞敏，E-mail：pangmin2009@126.comPANG Min, E-mail: pangmin2009@126.com
- 基金信息：
  
  山西省省筹资金资助回国留学人员科研项目(2022-191);山西省应用基础研究计划项目(202103021223433);山西医科大学第一医院136专项经费科研项目(2021-07)
- DOI：10.16016/j.2097-0927.202309135
  中图分类号： R322.34;R329.28;R977.6
- 收稿：2023-09-24，
  
  修回：2023-12-06，
  
  纸质出版：2024-06-30
- 稿件说明：
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李婷, 杨晓雪, 高睿, 等. 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[J]. 陆军军医大学学报, 2024,46(12):1410-1416.

Ting LI, Xiaoxue YANG, Rui GAO, et al. Recombinant human CC16 inhibits senescence in human bronchial epithelial cells induced by cigarette smoke extract[J]. Journal of Army Medical University, 2024, 46(12): 1410-1416.
李婷, 杨晓雪, 高睿, 等. 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[J]. 陆军军医大学学报, 2024,46(12):1410-1416. DOI： 10.16016/j.2097-0927.202309135.

Ting LI, Xiaoxue YANG, Rui GAO, et al. Recombinant human CC16 inhibits senescence in human bronchial epithelial cells induced by cigarette smoke extract[J]. Journal of Army Medical University, 2024, 46(12): 1410-1416. DOI： 10.16016/j.2097-0927.202309135.

摘要

目的

探讨重组人CC16蛋白质(rhCC16)对香烟烟雾提取物(cigarette smoke extract

CSE)诱导的人支气管上皮细胞(human bronchial epithelial cells

HBECs)衰老的抑制作用及机制。

方法

CCK-8法检测CSE (0%、1%、2.5%、5%、7.5%和10%)及rhCC16(0、10、100、250和500 ng/mL)对HBECs细胞活力的影响; β-半乳糖苷酶染色试剂盒检测对照组、CSE组以及CSE+rhCC16组细胞β-半乳糖苷酶活性; 实时荧光定量PCR (qPCR

)检测各组细胞

16、

21 mRNA表达水平; Western blot检测各组细胞P16、P21、p-P53、P38、p-P38、ERK1/2、p-ERK1/2蛋白表达水平。

结果

与对照组相比

5% CSE刺激细胞72 h对HBECs细胞活力无显著影响; 500 ng/mL及以下浓度rhCC16对HBECs细胞活力无显著影响; 与对照组相比

5% CSE刺激HBECs细胞72 h致β-半乳糖苷酶染色阳性细胞率明显升高(

0.05)

且P16和P21蛋白和mRNA表达水平明显升高(

0.05)

p-P53、p-P38与p-ERK1/2蛋白表达量显著增加(

0.05);与CSE组相比

250 ng/mL rhCC16干预下

HBECs细胞β-半乳糖苷酶染色阳性细胞率显著下降(

0.05)

P16和P21蛋白和mRNA表达水平显著下降(

0.05)

p-P53、p-p38和p-ERK1/2的表达量降低(

0.05)。

结论

rhCC16蛋白质抑制香烟烟雾诱导的HBECs衰老

抑制P38 MAPK和ERK1/2信号通路可能是其作用机制。

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%

2.5%

7.5% and 10% CSE and/or 0

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

16 and

21 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 (

0.05)

elevated mRNA and protein levels of P16 and P21(

0.05)

and enhanced protein levels of p-P53

p-P38 and p-ERK1/2(

0.05) when compared with the control group.Compared with the simple CSE stimulation

250 ng/mL rhCC16 treatment decreased positive rate to β-galactosidase staining (

0.05)

reduced mRNA and protein levels of P16 and P21(

0.05) and protein levels of p-P53

p-P38 and p-ERK1/2(

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.

关键词

Keywords

references

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