Kyungheechunggan-Tang-01, a New Herbal Medication, Suppresses LPS-Induced Inflammatory Responses through JAK/STAT Signaling Pathway in RAW 264.7 Macrophages

• Published in: Evidence-based complementary and alternative medicine 2017-01, Vol.2017 (2017), p.1-15
• Main Authors: Lee, Kyung-Tae, Park, Geonha, Lee, Jang-Hoon, Inn, Kyung-Soo, Shin, Ji-Sun, Jang, Eungyeong, Han, Hee-Soo, Jang, Young Pyo
• Format: Article
• Language: English
• Subjects: Activation; Anti-inflammatory agents; Biochemistry; Cyclooxygenase-2; Cytokines; Edema; Enzymes; Exploration; Gene expression; Genetic research; Health aspects; Herbal medicine; Immune system; Inflammation; Inflammatory diseases; Interleukin 6; Kinases; Ligands; Lipopolysaccharides; Macrophages; Mediation; Medicinal plants; Medicine, Botanic; Medicine, Herbal; mRNA; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Nutrition research; Pharmaceuticals; Pharmacy; Phosphorylation; Physiology; Prostaglandin E2; Rodents; Signal transduction; Stat3 protein; Tissues; Transcription factors; Tumor necrosis factor; Tumor necrosis factor-TNF; Tumor necrosis factor-α
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2017/7383104

Medicinal plants have been used as alternative therapeutic tools to alleviate inflammatory diseases. The objective of this study was to evaluate anti-inflammatory properties of Kyungheechunggan-tang- (KCT-) 01, KCT-02, and Injinchunggan-tang (IJCGT) as newly developed decoctions containing 3–11 herbs in LPS-induced macrophages. KCT-01 showed the most potent inhibitory effects on LPS-induced NO, PGE2, TNF-α, and IL-6 production among those three herbal formulas. In addition, KCT-01 significantly inhibited LPS-induced iNOS and COX-2 at protein levels and expression of iNOS, COX-2, TNF-α, and IL-6 at mRNA levels. Molecular data revealed that KCT-01 attenuated the activation of JAK/STAT signaling cascade without affecting NF-κB or AP-1 activation. In ear inflammation induced by croton oil, KCT-01 significantly reduced edema, MPO activity, expression levels of iNOS and COX-2, and STAT3 phosphorylation in ear tissues. Taken together, our findings suggest that KCT-01 can downregulate the expression of proinflammatory genes by inhibiting JAK/STAT signaling pathway under inflammatory conditions. This study provides useful data for further exploration and application of KCT-01 as a potential anti-inflammatory medicine.