Suppression of Baeckea frutescens L. and its components on MyD88-dependent NF-κB pathway in MALP-2-stimulated RAW264.7 cells

Baeckea frutescens L. 及其成分对 MALP-2 刺激的 RAW264.7 细胞中 MyD88 依赖的 NF-κB 通路的抑制

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作者:Qin-Wei Yu, Hao Wang, Jing-Ting Huo, Xiao-Fei An, Peng Gao, Zhen-Zhou Jiang, Lu-Yong Zhang, Ming Yan

Conclusion

The results of this study indicated that Baeckea frutescens L. and its components could inhibit the anti-infectious inflammatory events and iNOS expression in MALP-2 stimulated RAW264.7 cells. Among them, BF-2 might play a role through the inhibition of the MyD88 and NF-κB pathway. Our study might provide a new strategy to design and develop this kind of drug towards mycoplasma-infected inflammation.

Methods

The anti-infectious inflammation of Baeckea frutescens L. were studied by using macrophage activating lipopeptide-2 (MALP-2)-stimulated RAW264.7 cell model in vitro. Secretion of nitric oxide (NO), expression of inducible NO synthase (iNOS) and cytokines were detected as classic inflammatory index. Expression of Myeloid differentiation factor 88 (MyD88), degradation of inhibitory κBα (IκBα) and nuclear translocation of NF-κB p65 were further investigated.

Results

The results suggested that Baeckea frutescens L. has effect on suppression of MALP-2-mediated inflammation in RAW264.7 cells. The secretion of NO and the expression of iNOS could be inhibited. The secretion of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were also declined. Baeckea frutescens L. significantly decreased the expression of MyD88, therefore, inhibited the degradation of IκBα, reduced the level of nuclear translocation of p65.

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