4.7 Article

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

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 267, Issue -, Pages -

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2020.113497

Keywords

Sheng-Mai Yin; LPS; Anti-inflammatory; RAW 264.7 cell; Zebrafish

Funding

  1. National Science Foundation of China [81730110, 81973544, 81903886, 82074116]
  2. Guangzhou Education Bureau University Scientific Research project [201831845]
  3. Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (GDHVPS2018)
  4. Guangdong Basic and Applied Basic Research Foundation [2019A1515010821]
  5. China Postdoctoral Science Foundation [2019M652988]
  6. Young Elite Scientists Sponsorship Program by CACM [2019-QNRC2-C14]

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This study found that Sheng-Mai Yin has significant anti-inflammatory effects, potentially achieved through inhibiting the NF-kappa B and STAT3 signal pathways.
Ethnopharmacological relevance: 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. Materials and methods: The levels of pro-inflammatory cytokines IL-6 and TNF-alpha secreted by RAW 264.7 cells were measured by ELISA. The protein expressions of I kappa B alpha, p-I kappa B alpha (Ser32), STAT3 and p-STAT3 (Tyr705) were determined by Western blotting. And the nuclear translocation of NF-kappa B 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. Results: SMY reduced the release of IL-6 and TNF-alpha, inhibited the phosphorylation of I kappa B alpha and STAT3 as well as the nuclear translocation of NF-kappa B 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-kappa B, I kappa B alpha and STAT3 in zebrafish inflammatory models. Conclusion: SMY exerts significant anti-inflammatory effects with a potential mechanism of inhibiting the NF-kappa B and STAT3 signal pathways. Our findings suggest a scientific rationale of SMY to treat inflammatory diseases in clinic.

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