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International Journal of Pharmacology

Year: 2020 | Volume: 16 | Issue: 8 | Page No.: 542-553
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Authors

JunChao Peng

YuKun Wang

XueYan Xie

Qiong Yi

Xin Li

YuHao Wei

XuHua He

Lu Wang

Lu Wang

Keywords

Background and Objective: Both leukocyte differentiation antigen 14 (CD14) and myeloid differentiation protein-2 (MD-2) contain hydrophobic vesicles for extracting and delivering lipopolysaccharide (LPS), which play an irreplaceable role in the extracellular signal transduction of LPS. Chlorogenic acid (CGA) is a phenolic compound with a strong anti-inflammatory effect. However, it is currently unclear whether CGA blocks the extracellular signal transmission of LPS by occupying the hydrophobic pockets of CD14 and MD-2. Materials and Methods: Flow cytometry and siRNA were used to detect the presence of CD14 and MD-2 on breast epithelial cells (MECs). Molecular docking, Western blot, reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were used to study the targeting effect of CGA on CD14 and MD-2 and its influence on cytokine secretion. The protective effect of CGA on breast inflammation was observed under a transmission electron microscope. Results: The results showed that MD-2 and CD14 were expressed on MECs. When CD14 and MD-2 are inhibited alone or at the same time, the binding rate of LPS and MECs and the secretion of cytokines are reduced. CGA can not only occupy the hydrophobic vesicles of CD14 and MD-2, block the extracellular signal transmission of LPS but also inhibit the expression of CD14 and MD-2, thereby blocking the signal transmission of LPS from extracellular to intracellular. Conclusion: Besides, CGA can effectively inhibit the general changes of breast tissue, breast inflammatory cell infiltration, mitochondria and rough endoplasmic reticulum damage caused by lipopolysaccharide. In conclusion, CGA is expected to act as an antagonist of CD14 and MD-2 to inhibit mastitis.
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