ATTENUATION OF CIGARETTE-SMOKE-INDUCED OXIDATIVE STRESS BY OAT DIET
DOI:
https://doi.org/10.24269/ijhs.v8i1.6599Abstract
Even after cessation of cigarette smoke exposure, long-term exposure leads to lung fibrous tissue growth characteristically by oxidative stress. Oat, an inexpensive dietary source with antioxidant characteristics, is expected to alleviate oxidative stress in the lung tissue after exposure to cigarette smoke has ceased. This research aims to evaluate the effect of an oat diet in alleviating oxidative stress in the lung tissue of BALB/c mice after cessation of cigarette smoke exposure. A randomized post-test-only control group design was used for this research. The sample used in this experiment is male BALB/c mice (n = 33). Mice with BALB/c strain were separated into two groups: (1) control and (2) treatment. SOD, GSH, and MDA were the variables of the study. Cigarette smoke exposure decreases the activity of SOD and GSH and increases the concentration of MDA. After cigarette smoke exposure had been stopped in the oat-treated mice group, SOD and GSH activities were enhanced, and the MDA content dropped. This research's variable outcomes were statistically significant (P<0.05) from the standard feed alone-treated BALB/c mice group. Thus, consuming oats may alleviate oxidative stress implicated in lung fibrogenesis following cessation of tobacco smoke exposure
References
[2] M. Andersson, P. D. Blanc, K. Torén, and B. Järvholm, “Smoking, occupational exposures, and idiopathic pulmonary fibrosis among Swedish construction workers,†Am J Ind Med, vol. 64, no. 4, pp. 251–257, Apr. 2021, doi: 10.1002/ajim.23231.
[3] T. Zaman and J. S. Lee, “Risk Factors for the Development of Idiopathic Pulmonary Fibrosis: a Review,†Curr Pulmonol Rep, vol. 7, no. 4, pp. 118–125, Dec. 2018, doi: 10.1007/s13665-018-0210-7.
[4] L. Fang et al., “Cigarette smoke exposure combined with lipopolysaccharides induced pulmonary fibrosis in mice,†Respir Physiol Neurobiol, vol. 266, pp. 9–17, Aug. 2019, doi: 10.1016/j.resp.2019.04.010.
[5] N. I. Winters, A. Burman, J. A. Kropski, and T. S. Blackwell, “Epithelial Injury and Dysfunction in the Pathogenesis of Idiopathic PulmonaryFibrosis,†Am J Med Sci, vol. 357, no. 5, pp. 374–378, May 2019, doi: 10.1016/j.amjms.2019.01.010.
[6] L. Zuo et al., “Interrelated role of cigarette smoking, oxidative stress, and immune response in COPD and corresponding treatments,†American Journal of Physiology-Lung Cellular and Molecular Physiology, vol. 307, no. 3, pp. L205–L218, Aug. 2014, doi: 10.1152/ajplung.00330.2013.
[7] A. C. Schamberger, C. A. Staab-Weijnitz, N. Mise-Racek, and O. Eickelberg, “Cigarette smoke alters primary human bronchial epithelial cell differentiation at the air-liquid interface,†Sci Rep, vol. 5, no. 1, p. 8163, Feb. 2015, doi: 10.1038/srep08163.
[8] S. Sang and Y. F. Chu, “Whole grain oats, more than just a fiber: Role of unique phytochemicals,†Mol Nutr Food Res, vol. 61, no. 7, p. 1600715, Jul. 2017, doi: 10.1002/MNFR.201600715.
[9] Q. Wang and P. R. Ellis, “Oat β-glucan: physico-chemical characteristics in relation to its blood-glucose and cholesterol-lowering properties,†Br J Nutr, vol. 112 Suppl 2, pp. S4–S13, Sep. 2014, doi: 10.1017/S0007114514002256.
[10] D. Paudel, B. Dhungana, M. Caffe, and P. Krishnan, “A Review of Health-Beneficial Properties of Oats,†Foods, vol. 10, no. 11, Nov. 2021, doi: 10.3390/FOODS10112591.
[11] M. L. Hernandez and D. B. Peden, “Air Pollution : Indoor and Outdoor,†in Middleton’s Allergy: Principles and Practice, 9th ed.2020, pp. 479–499.
[12] Y. A. Hajam et al., “Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives,†Cells, vol. 11, no. 3, p. 552, Feb. 2022, doi: 10.3390/cells11030552.
[13] A. G. Fois et al., “Evaluation of oxidative stress biomarkers in idiopathic pulmonary fibrosis and therapeutic applications: a systematic review,†Respir Res, vol. 19, no. 1, p. 51, Dec. 2018, doi: 10.1186/s12931-018-0754-7.
[14] A. C. Mdgley et al., “Transforming Growth Factor-β1 (TGF-β1)-stimulated Fibroblast to Myofibroblast Differentiation Is Mediated by Hyaluronan (HA)-facilitated Epidermal Growth Factor Receptor (EGFR) and CD44 Co-localization in Lipid Rafts,†Journal of Biological Chemistry, vol. 288, no. 21, pp. 14824–14838, May 2013, doi: 10.1074/jbc.M113.451336.
[15] J. Krstić, D. Trivanović, S. Mojsilović, and J. F. Santibanez, “Transforming Growth Factor-Beta and Oxidative Stress Interplay: Implications in Tumorigenesis and Cancer Progression,†Oxid Med Cell Longev, vol. 2015, pp. 1–15, 2015, doi: 10.1155/2015/654594.
[16] C. Estornut, J. Milara, M. A. Bayarri, N. Belhadj, and J. Cortijo, “Targeting Oxidative Stress as a Therapeutic Approach for Idiopathic Pulmonary Fibrosis,†Front Pharmacol, vol. 12, Jan. 2022, doi: 10.3389/fphar.2021.794997.
[17] C. Bazzini et al., “Short- and Long- Term Effects of Cigarette Smoke Exposure on Glutathione Homeostasis in Human Bronchial Epithelial Cells,†Cellular Physiology and Biochemistry, vol. 32, no. 7, pp. 129–145, 2013, doi: 10.1159/000356633.
[18] I. Dalle-Donne et al., “Cigarette smoke and glutathione: Focus on in vitro cell models,†Toxicology in Vitro, vol. 65, p. 104818, Jun. 2020, doi: 10.1016/j.tiv.2020.104818.
[19] A. T. Figueiredo-Junior et al., “Treatment with Bixin-Loaded Polymeric Nanoparticles Prevents Cigarette Smoke-Induced Acute Lung Inflammation and Oxidative Stress in Mice,†Antioxidants, vol. 11, no. 7, p. 1293, Jun. 2022, doi: 10.3390/antiox11071293.
[20] P. Cheresh, S.-J. Kim, S. Tulasiram, and D. W. Kamp, “Oxidative stress and pulmonary fibrosis,†Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, vol. 1832, no. 7, pp. 1028–1040, Jul. 2013, doi: 10.1016/j.bbadis.2012.11.021.
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