Anti-Inflammatory Effect of Apigenin on LPS-Induced Pro-Inflammatory Mediators and AP-1 Factors in Human Lung Epithelial
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Anti-Inflammatory Effect of Apigenin on LPS-Induced Pro-Inflammatory Mediators and AP-1 Factors in Human Lung Epithelial Cells Rajeshwari H. Patil,1 R. L. Babu,1,2 M. Naveen Kumar,1 K. M. Kiran Kumar,1 Shubha M. Hegde ,1 Rashmi Nagesh,1 Govindarajan T. Ramesh,3 and S. Chidananda Sharma1,4
Abstract—Apigenin is one of the plant flavonoids present in fruits and vegetables, acting as an important nutraceutical component. It is recognized as a potential antioxidant, antimicrobial, and antiinflammatory molecule. In the present study, the mechanism of anti-inflammatory action of apigenin on lipopolysaccharide (LPS)-induced pro-inflammatory cytokines and activator protein-1 (AP-1) factors in human lung A549 cells was investigated. The anti‐inflammatory activity of apigenin on LPS-induced inflammation was determined by analyzing the expression of pro-inflammatory cytokines, nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and different AP-1 factors. Apigenin significantly inhibited the LPS-induced expression of iNOS, COX-2, expression of pro-inflammatory cytokines (IL-1β, IL-2, IL-6, IL-8, and TNF-α), and AP-1 proteins (c-Jun, c-Fos, and JunB) including nitric oxide production. Study confirms the anti-inflammatory effect of apigenin by inhibiting the expression of inflammatory mediators and AP-1 factors involved in the inflammation and its importance in the treatment of lung inflammatory diseases. KEY WORDS: apigenin; LPS; pro-inflammatory mediators; AP-1 factors; A549.
INTRODUCTION Inflammation is responsible for rheumatoid arthritis, atherosclerosis including asthma and other pathophysiological diseases. During an inflammatory response, mediators, such as pro-inflammatory cytokines (interleukin (IL) -1), IL-6, IL-12, IL-18), tumor necrosis factor (TNF-α), interferon (IFN)-γ and the granulocyte–macrophage colony-stimulating factors (GMCF) are released. Proinflammatory mediators are antagonized by antiinflammatory cytokines (IL-4, IL-10, IL-13) and transforming growth factor [1]. Among all the inflammatory 1
Department of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India 2 Department of Bioinformatics and Biotechnology, Karnataka State Women’s University, Jnanashakthi Campus, Vijayapura, 586 108, Karnataka, India 3 Department of Biology and Center for Biotechnology and Biomedical Sciences, Norfolk State University, Norfolk, VA, USA 4 To whom correspondence should be addressed at Department of Microbiology and Biotechnology, Bangalore University, Jnana Bharathi, Bengaluru, 560 056, Karnataka, India. E-mail: [email protected]
diseases, sepsis is potentially a fatal syndrome of irreversible cardiovascular collapse and critical organ failure due to systemic inflammatory state caused in response to circulating microbes or microbial toxins attributed to lipopolysaccharide (LPS) of gram-negative bacteria or bacterial DNA [2]. LPS is a potent activator of monocytes and macrophages, and different organ cell types stimulate the expression of cytokines including adh
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