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Sheng-Mai Yin exerts anti-inflammatory effects on RAW 264.7 cells and zebrafish
Yuanru Zheng1, Chunyang Tian1, Chunlin Fan2
1Traditional Chinese Pharmacological Laboratory, Third Level Research Laboratory of State Administration of Traditional Chinese Medicine, School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, 510515, PR China; Guangdong Provincial Key Laboratory of Chinese Medicine Pharmaceutics, Guangzhou, 510515, PR China.
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-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.
Results:
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.
Conclusion:
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.
