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SIRT3 调控支气管上皮细胞凋亡并加重哮喘气道炎症。

SIRT3 regulates bronchial epithelium apoptosis and aggravates airway inflammation in asthma.

机构信息

Department of Pulmonary and Critical Care Medicine, Beijing Luhe Hospital, Capital Medical University, Tongzhou, Beijing 101100, P.R. China.

出版信息

Mol Med Rep. 2022 Apr;25(4). doi: 10.3892/mmr.2022.12660. Epub 2022 Mar 2.

DOI:10.3892/mmr.2022.12660
PMID:35234263
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8915391/
Abstract

Sirtuin (SIRT)3 is closely related to inflammation and apoptosis and studies have described this relationship, including in the lungs. However, the expression of SIRT3 and its effect on apoptosis and inflammation in bronchial tissue in asthma remains to be elucidated. The present study found that SIRT3 expression decreased in the bronchial tissues of asthmatic mice and its upregulation could not only reduce increased bronchial epithelial cells apoptosis in the asthmatic mice but also significantly decreased the elevated expression of cytokines (TNF‑α, IL‑4, IL‑5 and IL‑13) in bronchoalveolar lavage fluid. Further study found that SIRT3 overexpression significantly decreased apoptosis‑related protein expression (Bax/Bcl2 ratio and caspase 3 activity) and oxidative injury. , SIRT3 regulated oxidative stress‑induced bronchial epithelial cell (16HBE) apoptosis and cytokine expression. In conclusion, SIRT3 expression decreased in bronchial tissues of asthmatic mice and the upregulation of SIRT3 expression could reduce the apoptosis of bronchial epithelium and airway inflammation. It was concluded that SIRT3 might be a potential target in asthma treatment.

摘要

Sirtuin (SIRT)3 与炎症和细胞凋亡密切相关,已有研究对此进行了描述,包括在肺部。然而,SIRT3 的表达及其对哮喘支气管组织中细胞凋亡和炎症的影响仍有待阐明。本研究发现,哮喘小鼠支气管组织中 SIRT3 表达降低,其上调不仅可以减少哮喘小鼠中支气管上皮细胞凋亡的增加,还可以显著降低支气管肺泡灌洗液中细胞因子(TNF-α、IL-4、IL-5 和 IL-13)的升高表达。进一步的研究发现,SIRT3 过表达可显著降低凋亡相关蛋白表达(Bax/Bcl2 比值和 caspase 3 活性)和氧化损伤。SIRT3 调节氧化应激诱导的支气管上皮细胞(16HBE)凋亡和细胞因子表达。综上所述,哮喘小鼠支气管组织中 SIRT3 表达降低,上调 SIRT3 表达可减少支气管上皮细胞凋亡和气道炎症。因此,SIRT3 可能是哮喘治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/03dd5ab74f46/mmr-25-04-12660-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/d077f1251807/mmr-25-04-12660-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/fb6e6b8bfd8f/mmr-25-04-12660-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/b455f0702155/mmr-25-04-12660-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/2a82ee1c9644/mmr-25-04-12660-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/9ba716679159/mmr-25-04-12660-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/03dd5ab74f46/mmr-25-04-12660-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/d077f1251807/mmr-25-04-12660-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/fb6e6b8bfd8f/mmr-25-04-12660-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/b455f0702155/mmr-25-04-12660-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/2a82ee1c9644/mmr-25-04-12660-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/9ba716679159/mmr-25-04-12660-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0a50/8915391/03dd5ab74f46/mmr-25-04-12660-g05.jpg

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