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Resveratrol decreases cell apoptosis through inhibiting DNA damage in bronchial epithelial cells

One of the major risk factors for asthma development is exposure to environmental allergens. House dust mites (HDM) can induce DNA damage, resulting in asthma. Resveratrol (RES) produced by several plants, has anti-apoptotic properties and may affect a variety of biological processes. The aim of the...

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Detalles Bibliográficos
Autores principales: Zhang, Yun, Guo, Linlin, Law, Betty Yuen-Kwan, Liang, Xiaobo, Ma, Ning, Xu, Guofeng, Wang, Xiaoyun, Yuan, Xiefang, Tang, Hongmei, Chen, Qi, Wong, Vincent Kam-Wai, Wang, Xing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7169938/
https://www.ncbi.nlm.nih.gov/pubmed/32186748
http://dx.doi.org/10.3892/ijmm.2020.4539
Descripción
Sumario:One of the major risk factors for asthma development is exposure to environmental allergens. House dust mites (HDM) can induce DNA damage, resulting in asthma. Resveratrol (RES) produced by several plants, has anti-apoptotic properties and may affect a variety of biological processes. The aim of the present study was to investigate the protective role of RES against apoptosis in bronchial epithelial cells. C57BL/6J mice treated with HDM exhibited high levels of cell apoptosis, while RES significantly reversed this process. Induced DNA damage was more severe in the HDM group vs. the HDM combined with RES group. This result was confirmed by immunostaining and western blot analysis of the protein expression of the DNA damage-related gene γH2AX, which was highly induced by HDM. In addition, treatment with RES protected bronchial epithelial cells exposed to HDM from DNA damage. RES decreases reactive oxygen species levels to inhibit oxidative DNA damage in bronchial epithelial cells. Furthermore, compared with the HDM group, induced cell apoptosis could be attenuated by RES in the group of combined treatment with RES and HDM. A DNA repair inhibitor augmented DNA damage and apoptosis in bronchial epithelial cells, whereas RES significantly attenuated cell apoptosis through inhibiting DNA damage.