Sheng-Mai Yin exerts anti-inflammatory effects on RAW 264.7 cells and zebrafish

• Published in: Journal of ethnopharmacology Vol. 267; p. 113497
• Main Authors: Zheng, Yuanru, Tian, Chunyang, Fan, Chunlin, Xu, Nishan, Xiao, Junjie, Zhao, Xiaoyang, Lu, Zibin, Cao, Huihui, Liu, Junshan, Yu, Linzhong
• Format: Journal Article
• Language: English
• Published: Ireland Elsevier B.V 01.03.2021
• Subjects: Animals; Animals, Genetically Modified; Anti-inflammatory; Anti-Inflammatory Agents - pharmacology; Copper Sulfate; Cytokines - metabolism; Disease Models, Animal; Drug Combinations; Drugs, Chinese Herbal - pharmacology; Inflammation - chemically induced; Inflammation - immunology; Inflammation - metabolism; Inflammation - prevention & control; Inflammation Mediators - metabolism; Lipopolysaccharides; LPS; Macrophages - drug effects; Macrophages - immunology; Macrophages - metabolism; Mice; Neutrophil Infiltration - drug effects; Neutrophils - drug effects; Neutrophils - immunology; Neutrophils - metabolism; NF-kappa B - metabolism; NF-KappaB Inhibitor alpha - metabolism; RAW 264.7 cell; RAW 264.7 Cells; Sheng-Mai Yin; Signal Transduction; STAT3 Transcription Factor - metabolism; Zebrafish; Zebrafish - embryology; Zebrafish - genetics; Zebrafish Proteins - metabolism; Ser; DMSO; MTT; MPO; LPS; GFP; NF-κB; ANOVA; dpf; HPLC; hpi; PBS; BCA; Sheng-Mai Yin; H&E; qRT-PCR; STAT3; Zebrafish; DAPI; Tyr; IL-6; IκBα; ECL; TNF-α; RAW 264.7 cell; Dex; SEM; Anti-inflammatory; SMY; ELISA
• ISSN: 0378-8741; 1872-7573
• DOI: 10.1016/j.jep.2020.113497

Sheng-Mai Yin (SMY), a famous traditional Chinese medicine formula, has been commonly used in China for centuries to treat various diseases, such as inflammation-related diseases. However, the anti-inflammatory activity of SMY and its potential mechanisms still have not yet been clearly understood. Aim of the study: In this study, we aimed to determine the anti-inflammatory effect of SMY and explore its underlying mechanisms both on RAW 264.7 cells and zebrafish. The levels of pro-inflammatory cytokines IL-6 and TNF-α secreted by RAW 264.7 cells were measured by ELISA. The protein expressions of IκBα, p-IκBα (Ser32), STAT3 and p-STAT3 (Tyr705) were determined by Western blotting. And the nuclear translocation of NF-κB p65 in LPS-induced RAW 264.7 macrophage cells was detected by confocal microscopy. Moreover, the in vivo anti-inflammatory effect of SMY and its potential mechanisms were further investigated by survival analysis, hematoxylin-eosin staining (H&E), observation of neutrophil migration and quantitative real-time PCR (qRT-PCR) analysis in zebrafish inflammatory models. SMY reduced the release of IL-6 and TNF-α, inhibited the phosphorylation of IκBα and STAT3 as well as the nuclear translocation of NF-κB p65 in LPS-induced RAW 264.7 cells. Furthermore, the increased survival, decreased infiltration of inflammatory cells and the attenuated migration of neutrophils together suggested the in vivo anti-inflammatory effects of SMY. More importantly, SMY reduced the gene expressions of pro-inflammatory cytokines and suppressed LPS-induced up-regulation of NF-κB, IκBα and STAT3 in zebrafish inflammatory models. SMY exerts significant anti-inflammatory effects with a potential mechanism of inhibiting the NF-κB and STAT3 signal pathways. Our findings suggest a scientific rationale of SMY to treat inflammatory diseases in clinic. [Display omitted]