NDLI: Resveratrol exerts an anti-apoptotic effect on human bronchial epithelial cells undergoing cigarette smoke exposure.

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Resveratrol exerts an anti-apoptotic effect on human bronchial epithelial cells undergoing cigarette smoke exposure.

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Resveratrol exerts an anti-apoptotic effect on human bronchial epithelial cells undergoing cigarette smoke exposure.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Li, Yuping Ma, Miao Xie, Wang Yuan, Ting Zhang, Li Guo, Xialing Luo, Bailing
Description	Author Affiliation: Zhang L ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.); Guo X ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.); Xie W ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.); Li Y ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.); Ma M ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.); Yuan T ( Department of Critical Emergency Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410007, P.R. China.); Luo B ( Department of Respiratory Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.)
Abstract	Cigarette smoke can cause endoplasmic reticulum stress and induce apoptosis, both of which are important pathogenic factors contributing to chronic obstructive pulmonary disease. The aim of the present study was to produce a cigarette smoke extract (CSE)induced apoptosis human bronchial epithelial cell (HBEpC) model, to investigate the protective effects of resveratrol (RES). The role of oxygenregulated protein 150 (ORP150) in the RESinduced activation of Sirtuin 1 (SIRT1) was additionally studied. Cultured HBEpCs were initially treated with CSE to induce apoptosis, followed by an incubation either with or without RES. Numerous techniques were used to evaluate the outcomes of the present study, including cell counting kit8 assay, quantitative polymerase chain reaction, western blotting, Hoechst 33342 staining and AnnexinVPI flow cytometry apoptosis analyses, and gene knockdown. It was identified that 24 h 2% CSE incubation induced apoptosis in HBEpC, accompanied by an overexpression of the apoptosis molecular markers CCAATenhancerbinding protein homologous protein, caspase 4 and caspase 3. Pretreatment of the cells with RES markedly alleviated the severity of apoptosis, as confirmed by apoptosis analyses and the expression levels of the apoptosis molecular markers. SIRT1 was shown to be overexpressed following RES treatment. However, following the gene knockdown of ORP150, the antiapoptotic effects of RES were significantly attenuated. The results of the present study demonstrate that RES may have a protective effect against CSEinduced apoptosis, and a molecular pathway involving SIRT1 and ORP150 may be associated with the antiapoptotic functions of RES in HBEpC.
ISSN	17912997
e-ISSN	17913004
DOI	10.3892/mmr.2014.2925
Journal	Molecular Medicine Reports
Issue Number	3
Volume Number	11
Language	English
Publisher	Spandidos Publications
Publisher Date	2015-03-01
Publisher Place	Greece
Access Restriction	Open
Subject Keyword	Apoptosis Drug Effects Epithelial Cells Metabolism Respiratory Mucosa Cytology Adverse Effects Smoking Stilbenes Pharmacology Genetics Cell Line Gene Knockout Techniques Hsp70 Heat-shock Proteins Protective Agents Rna Interference Rna, Small Interfering Sirtuin 1 Research Support, Non-u.s. Gov't Discipline Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Genetics Biochemistry Molecular Biology Cancer Research Molecular Medicine Oncology

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