PPAR-alpha agonist (fenofibrate) therapy in exacerbation control of chronic obstructive pulmonary disease of severe stage
О. А. Еникеев, Svetlana Achmetovna Enikeeva, Nelya Raatovna Bikmetova
Abstract
О. А. Еникеев, Svetlana Achmetovna Enikeeva, Nelya Raatovna Bikmetova
Abstract
Aim: To study the influence of the therapy PPAR-alpha agonist (fenofibrate) in exacerbation dynamics of severe stage of chronic obstructive pulmonary disease (AECOPD) patients. Methods: Peripheral blood samples were collected from 20 patients with severe AECOPD receiving conventional therapy with 145 mg fenofibrate (1 tablet once a day No. 10) and 21 patients with severe AECOPD and 20 man from control group. Lymphocytes were isolated by two-color labeled monoclonal antibodies flow cytometry to examine the quantities and percentage of, CD3+CD19- T cell, CD3-CD19+ B cell, CD3+CD4+ T cell, CD3+CD8+ T cell, respectively. Enzyme immunodetection was used to detect the expression of tumor necrosis factor α (TNF-α). All patients underwent a spirography with broncholytic breakdown. Mann-Whitney test was used for comparison between data before and after treatment an control group. Results: Complex therapy with inclusion of fenofibrate significantly increased the indicators of TNF-a, compared with conventional therapy (p<0.05). This increase was accompanied by a significant increase in levels of FVC, FEV1/FVC, MEF75, MEF 25 and VC MAX, compared with the group receiving conventional therapy (p<0.05). Conclusion: Fenofibrate in addition to the direct immunomodulating effect, significantly improves the function of external respiration. Statistically significant increase in the level of TNF-alpha may be associated with activation of apoptosis phagocytic cells, leading to the limitation of the systemic inflammatory response in the body.
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Aim: To study the influence of the therapy PPAR-alpha agonist (fenofibrate) in exacerbation dynamics of severe stage of chronic obstructive pulmonary disease (AECOPD) patients. Methods: Peripheral blood samples were collected from 20 patients with severe AECOPD receiving conventional therapy with 145 mg fenofibrate (1 tablet once a day No. 10) and 21 patients with severe AECOPD and 20 man from control group. Lymphocytes were isolated by two-color labeled monoclonal antibodies flow cytometry to examine the quantities and percentage of, CD3+CD19- T cell, CD3-CD19+ B cell, CD3+CD4+ T cell, CD3+CD8+ T cell, respectively. Enzyme immunodetection was used to detect the expression of tumor necrosis factor α (TNF-α). All patients underwent a spirography with broncholytic breakdown. Mann-Whitney test was used for comparison between data before and after treatment an control group. Results: Complex therapy with inclusion of fenofibrate significantly increased the indicators of TNF-a, compared with conventional therapy (p<0.05). This increase was accompanied by a significant increase in levels of FVC, FEV1/FVC, MEF75, MEF 25 and VC MAX, compared with the group receiving conventional therapy (p<0.05). Conclusion: Fenofibrate in addition to the direct immunomodulating effect, significantly improves the function of external respiration. Statistically significant increase in the level of TNF-alpha may be associated with activation of apoptosis phagocytic cells, leading to the limitation of the systemic inflammatory response in the body.
Key concepts: Medicine, Fenofibrate, Exacerbation, CD8, Gastroenterology, Internal medicine, CD3, CD19