Carcinogenesis, Teratogenesis & Mutagenesis ›› 2020, Vol. 32 ›› Issue (2): 92-97.doi: 10.3969/j.issn.1004-616x.2020.02.003

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1,25-(OH)2D3 attenuates PM2.5-induced oxidative stress in HBE cells

SUN Jiaojiao, CHE Bizhong, LUO Qiulin, ZHAI Bingzhong, XIN Lili   

  1. School of Public Health, Medical College of Soochow University, Suzhou 215123, Jiangsu, China
  • Received:2019-05-16 Revised:2019-12-05 Online:2020-03-30 Published:2020-04-10

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Abstract: OBJECTIVE: The aim of this study was to investigate whether 1,25-dihydroxyvitamin D3[1,25-(OH)2D3] would inhibit oxidative damage which was induced by PM2.5 in human bronchial epithelial cells (HBE). METHODS: HBE cells were divided into four groups:vehicle (ethanol,0.1%) control,1,25-(OH)2D3-treated group,ethanol + PM2.5-treated group,and PM2.5+1,25-(OH)2D3-treated group. HBE cells were pretreated with ethanol (0.1%) or 1×10-9 mol/L of 1,25-(OH)2D3 for 24 h. Afterwards,the cell culture medium was replaced with medium containing PM2.5 (200 μg/mL) and ethanol (0.1%) or PM2.5 (200 μg/mL) and 1×10-9 mol/L 1,25-(OH)2D3. After another 24 hours of incubation of the cultures,cells were harvested for determination of cell viability,MDA concentrations,ratios of reduced glutathione (GSH) to oxidized glutathione (GSSG),and expression levels of transcription factor NF-E2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1) protein. These expressions were detected using CCK-8 assay kit,cell MDA assay kit,GSH/GSSG-GloTM assay kit,and Western blot,respectively. RESULTS: In the PM2.5-treated groups,the cell viabilities were obviously decreased to 80.8% as compared with the control. After 48-h treatment of 1,25-(OH)2D3, the viability of PM2.5-treated HBE cells was further reduced to 75.8%. After PM2.5 exposure,MDA concentrations were significantly increased (P < 0.05),and the ratios of GSH/GSSG were found to be decreased significantly (P < 0.01) as compared with the control. After 48 h-treatment with 1,25-(OH)2D3, the anti-oxidative levels in the PM2.5-exposed group were significantly improved (P < 0.05),together with decreased MDA concentrations and increased GSH/GSSG ratios. Protein analyses reveal that PM2.5 could increase levels of Nrf-2 and HO-1 proteins in HBE cells. The 48 h-intervention of 1,25-(OH)2D3 could up-regulate VDR level and slightly increased levels of Nrf-2 and HO-1 in PM2.5-treated HBE cells. CONCLUSIONS:PM2.5 exposure induced oxidative damage in HBE cells,together with elevated lipid peroxidation,decreased GSH/GSSG ratios,and increased levels of antioxidant proteins including Nrf-2 and HO-1 proteins. However,1,25-(OH)2D3 exposure attenuated PM2.5-induced oxidative stress,probably through regulation of Nrf-2/HO-1 pathway via VDR. Furthermore,1,25-(OH)2D3 exposure attenuated PM2.5-induced oxidative stress,probably related to VDR and Nrf-2/HO-1 signal pathways. Finally,1,25-(OH)2D3 exposure decreased cell viability,probably attributed to cell cycle arrest,and PM2.5-induced cell apoptosis which was promoted by 1,25-(OH)2D3.

Key words: PM2.5, 1,25-(OH)2D3, oxidative stress, Nrf-2, HO-1

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