The Effects of Quercetinon Interleuikin (IL-8) Serum, %Forced Expiratory Volume in One Second (FEV1), and COPD Assessment Test (CAT) Scores in Stable Chronic Obstructive Pulmonary Disease (COPD) Patients
DOI:
https://doi.org/10.36497/jri.v39i2.51Keywords:
stable COPD, quercetin, IL-8 serum, ?V1, CAT scoreAbstract
Introduction: Chronic obstructive pulmonary disease (COPD) is the leading cause of morbidity and mortality worldwide. Cigarette smoke and noxious agent result in oxidative stress and activate release of inflammatory mediators such as Interleukin-8 (IL-8). Quercetin is a flavonoid compound containing anti-inflammatory effects which can be used as an adjuvant therapy in stable COPD. Objective: To analyze the effect of quercetin on serum IL-8 levels, % VEP1, and CAT score of stable COPD patients. Methods: Experimental clinical trial with pre-test and pasca-test design was performed in 30 patients with stable COPD in Dr. Moewardi Surakarta between December 2017 and January 2018. The samples taken by using purposive sampling were divided into two groups treatment groups received standard therapy and quercetin 500mg/day for 28 days and control groups only received standard therapy. The decrease in inflammation was measured by serum IL-8 examination, improvement of obstruction measured by %FEV1 and clinical improvement measured by CAT score. Results: IL-8 serum level was significantly lower in treatment group than of in control group (p=0,001). The percentage of FEV1 was insignificant different between the two group (p=0,236). However CAT score was significantly lower in treatment group compared to that of in control group (p=0,001) Conclusions: Quercetin can decrease IL-8 serum level and decrease CAT score when given in combination with standard therapy for COPD patients. (J Respir Indo 2019; 39(2): 103-12)Downloads
References
Perhimpunan Dokter Paru Indonesia. Penyakit paru obstruktif kronik (PPOK). Pedoman praktis dan penatalaksanaan di Indonesia. Jakarta: Per- himpunan Dokter Paru Indonesia; 2016. p. 1-111.
Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, manage- ment, and prevention of chronic obstructive pul- monary disease. Capetown: Global Initiative for Chronic Obstructive Lung Disease Inc; 2017. p. 1-123.
MacNee W. COPD: pathology, pathogenesis, and pathophysiology. In: Currie G, editor. ABC of COPD. 1st ed. New York: Blackwell Publishing Company; 2006. p. 1202-30.
Chung KF, Adcock IM. Multifaceted mechanism in COPD: Inflammation, immunity, and tissue repair and destruction. Eur Respir J. 2008;31(6):1334-56.
Larsson K. Aspect on pathophysiological mecha- nism in COPD. Journal of Intern Med. 2007;262(3):311-40.
Barnes PJ. Mediators of chronic obstructive pulmonary disease. Pharmacol Rev. 2004;56(4):515-48.
Wedzicha JA, Brill SE, Allinson JP, Donaldson GC. Mechanism and impact of the frequent exacerbator phenotype in chronic obstructive pulmonary disease. BMC. 2013;11(181):1-10.
Barnes P. Chronic obstructive pulmonary disease: effects beyond the lungs. PLOS Med. 2010;7(3):1-4.
Barnes PJ. New anti-inflammatory targets for chronic obstructive pulmonary disease. Nat Rev Drug Discov. 2013;12:543-59.
Tabak C, Arts IC, Smit HA, Heederik D, Kromhout D. Chronic obstructive pulmonary disease and intake of catechins, flavonols, and flavones. The Morgen Study. AM J Crit Care. 2001;164:61-4.
Ganesan S, Faris AN, Comstock AT, Chattoraj SS, Chattoraj A, Burgess JR, et al. Quercetin prevents progression of disease in elastase / LPS-exposed mice by negatively regulating MMP expression. Respir Res. 2010;11(131):1-15.
Alrawaiq NS, Abdullah A. A Review of flavonoid quercetin: metabolism, bioactivity and antioxidant properties. Int J PharmaTech Res. 2014;6(3):933-41.
Barnes PJ, Rennard S. Patophysiology of COPD. In: Barnes PJ, Drazen J, Rennard S, Thomson N, editors. Asthma and COPD: Basics Mechanism and Clinical Management. 1st Ed. San Diego: Elsevier Inc.; 2009. p. 425-44.
Rajendrasozhan S, Yang SR, Edirisinghe I, Yao H, Adenuga D, Rahman I. Deacetylases and NF-κβ in redoks regulation of cigarette smoke induced lung inflammation: implications in pathogenesis of COPD. Antioxid Redox Sign. 2008;10(4):799-811.
Li Y, Yao J, Han C, Yang J, Chaudry MT, Wang S, et al. Quercetin, Inflammation and Immunity. Nutrients. 2016;8(3):1-14.
Apriningsih H. Pengaruh Epigallocatechin-3- Gallate Teh Hijau Terhadap Jumlah Netrofil Absolut Darah, Matrix Metalloproteinase-9 Serum, %VEP1, dan Nilai CAT Pasien PPOK stabil. [Tesis]. Universitas Sebelas Maret. Surakarta. 2016.
Nair MP, Mahajan S, Reynolds JL, Aalinkeel R, Nair H, Schwartz SA, et al. The flavonoid quercetin inhibits proinflammatory cytokine (Tumor Necrosis Factor Alpha) gene expression in normal peripheral blood mononuclear cells via modulation of the NF-kB System. Clin and Vaccine Immunol. 2006;13(3):319-28.
Sato M, Miyazaki T, Kambe F, Maeda K, Seo H. Quercetin, a biovalfonoid, inhibits the induction of interleukin 8 and monocyte chemoattractant protein-1 expression by tumor necrosis factor-alpha in cultured human synovial cells. JRheumathol. 1997;24(9):1680-4.
Barnes PJ. The cytokine network in chronic obstruvtive pulmonary disease. Am J Respir Cell Mol Biol. 2009;41:631-38.
Donohue JF, Jones PW, Bartels C, Marvel J, D’Andrea P, Banerji D, et al. Correlations between FEV1 and patient-reported outcomes: A pooled analysis of 23 clinical trials in patients with chronic obstructive pulmonary disease. Pulm Pharmacol Ther. 2017;12(5):1-28.
Downloads
Additional Files
Published
Issue
Section
License
- The authors own the copyright of published articles. Nevertheless, Jurnal Respirologi Indonesia has the first-to-publish license for the publication material.
- Jurnal Respirologi Indonesia has the right to archive, change the format and republish published articles by presenting the authors’ names.
- Articles are published electronically for open access and online for educational, research, and archiving purposes. Jurnal Respirologi Indonesia is not responsible for any copyright issues that might emerge from using any article except for the previous three purposes.