Research Article Anti-Inflammatory Effects of Aster incisus through the Inhibition of NF-κB, MAPK, and Akt Pathways in LPS-Stimulated RAW 264.7 Macrophages Daniel Ngabire, 1 Yeong-Ae Seong, 1 Maheshkumar Prakash Patil, 1 Irvine Niyonizigiye, 1 Yong Bae Seo, 2 and Gun-Do Kim 1 1 Department of Microbiology, College of Natural Sciences, Pukyong National University, Busan, Republic of Korea 2 Institute of Marine Biotechnology, College of Natural Sciences, Pukyong National University, Busan, Republic of Korea Correspondence should be addressed to Gun-Do Kim; gundokim@pknu.ac.kr Received 5 June 2018; Revised 18 September 2018; Accepted 3 October 2018; Published 29 November 2018 Academic Editor: Tânia Silvia Fröde Copyright © 2018 Daniel Ngabire et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Aster incisus is a common flower found in almost all regions of South Korea. In the current study, we investigated the potential antioxidant and anti-inflammatory properties of the Aster incisus methanol extract in LPS-stimulated RAW 264.7 cells. We analyzed the phytochemicals contained in the extract by GC-MS. GC-MS results showed that the Aster incisus extract contains 9 known compounds. Later on, DPPH assay, WST-1 assay, nitric oxide (NO) assay, Western blot, and RT-PCR were conducted to investigate the anti-inflammatory effects of the extract. Our WST-1 assay results revealed that Aster incisus did not affect the viability of all tested cell lines up to a concentration of 200 μg/ml; therefore, lower concentrations (50 μg/ml and 150 μg/ml) were used for further assays. Aster incisus scavenged DPPH and inhibited the production of NO. Aster incisus also reduced significantly the production of inflammation-related enzymes (iNOS, Cox-2) and cytokines (TNFα, IL-1β, and IL-6) and the gene expression of the proinflammatory cytokines. Additionally, further Western blot results indicated that Aster incisus inhibited the expression of p-PI3K, p-IκBα, p-p65 NF-κB, p-ERK1/2, p-SAPK/JNK, and p-Akt. Our results demonstrated that Aster incisus suppressed the expression of the inflammation mediators through the regulation of NF-κB, MAPK, and Akt pathways. 1. Introduction Inflammation is usually described as a defense mechanism used by animals to fight intruders. Inflammation can be divided into acute inflammation, which is a quick and short immune response, and chronic inflammation, which takes time to set up and may result in failure to remove the initial cause [1]. It can be related to a large number of serious diseases, like diabetes, cardiovascular disorders, Alzheimer’s disease, autoimmune and pulmonary diseases, arthritis, and cancer [2]. Immune cells, especially macrophages, play a major part in the nonspecific immunity against foreign intruders, specifically infectious microorganisms (bacteria, viruses, mycoplasma, etc.) [3–5]. Their activation during chronic inflammation is very crucial and sometimes associated with complications of chronic inflammation-related diseases by excessive production of nitric oxide (NO) and prostaglandin E2 (PGE2) or other inflammation-related cytokines [6–10]. Previously published papers have described the impor- tance of NF-κB, MAPK, and Akt pathways in the expression of mediators specific to inflammation [11–14]. Aster incisus is a species of the Asteraceae family and belongs to the Aster genus which contains approximately 248 to 706 species. Aster incisus is native to China, Japan, and Korea [15]. Recently, we reported the anticancer effects of Aster inci- sus on gastric adenocarcinoma. [16]. Other plants belonging to the Asteraceae family have been used for traditional medicinal purposes, and most recently, plants from the Aster genus were studied and reported for their anti-inflammatory effects [17] and other biological activities [18–22]. Hindawi Mediators of Inflammation Volume 2018, Article ID 4675204, 10 pages https://doi.org/10.1155/2018/4675204