Polygalaxanthone III downregulates inflammation in the lipopolysaccharide-stimulated RAW264.7 macrophages: A quantibody array analysis

• Published in: Journal of pharmacological sciences Vol. 147; no. 2; pp. 184 - 191
• Main Authors: Wu, Yinan, Fu, Hongwei, Yang, Xiaobin, Leng, Fang, Huang, Yadong, Deng, Hong, Xiang, Qi, Zhang, Shu
• Format: Journal Article
• Language: English
• Published: Japan Elsevier B.V 01-10-2021; Elsevier
• Subjects: Animals; Anti-Inflammatory Agents; Cytokines - genetics; Cytokines - metabolism; Down-Regulation - drug effects; Drugs, Chinese Herbal - pharmacology; Gene Expression - drug effects; Glycosides - pharmacology; IL21; Inflammation - etiology; Inflammation - genetics; Inflammation Mediators - metabolism; Inflammation modulation; Interleukins - genetics; Interleukins - metabolism; Lipopolysaccharides - adverse effects; Mice; Nitric Oxide - genetics; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; Polygala - chemistry; Polygala japonica Houtt; Polygalaxanthone III; Quantibody array; RAW 264.7 Cells; Reactive Oxygen Species - metabolism; Signal Transduction - drug effects; Xanthones - pharmacology; IL21; Quantibody array; Inflammation modulation; Polygalaxanthone III; Polygala japonica Houtt
• ISSN: 1347-8613; 1347-8648
• DOI: 10.1016/j.jphs.2021.06.010

Polygala japonica Houtt. (PJ), a member of the Polygala L. family that is suggested to exhibit detoxification properties in traditional Chinese medicine, is often used to treat upper respiratory tract infections. The anti-inflammatory effects of four main components of PJ (POL, PS-XLIX, PS-E, and PS-F) were examined using the LPS(0.3 μg·mL−1)-stimulated RAW264.7 macrophage model. The levels of NO, ROS, and iNOS were examined to analyze the anti-inflammatory activity of POL. Additionally, the levels of extracellular inflammation-related cytokines and chemokines were measured using quantibody array. The KEGG pathway analysis was performed to examine the anti-inflammatory mechanism of POL. The levels of NO in the POL-pretreated group were significantly downregulated when compared with those in the PS-E-pretreated, PS-F-pretreated, and PS-XLIX-pretreated groups. POL significantly inhibited the changes of iNOS, ROS, and inflammatory factors caused by LPS stimulation (p < 0.001). The expression levels of IL21 and GM-CSF were examined using qPCR, while those of JAK-STAT signaling pathway-related proteins in the LPS-stimulated RAW264.7 macrophages were analyzed using western blotting. POL significantly downregulated the expression of IL-21 and GM-CSF. The anti-inflammatory mechanism of POL is mediated through the JAK-STAT pathway. Thus, this study demonstrated that POL is an anti-inflammatory component of PJ and elucidated its mechanism.