Effect of Phellodendrine on Inflammatory Response in Rats with Atopic Dermatitis by Regulating MCP-1/CCR2 Signaling Pathway
Objective To investigate the effect of Phellodendrine on inflammatory response in rats with atopic dermatitis(AD)and its mechanism.Methods AD rat model was established.The rats were separated into normal group,model group,low-dose Phellodendrine group,high-dose Phellodendrine group,Phellodendrine+macrophage chemoattractant protein-1(MCP-1)group.After the end of administration,the rats in each group were scored for skin lesions,and the number of scratches was recorded,HE staining was applied to observe pathological changes in skin tissue,Toluidine blue staining was applied to determine the number of Mast cells,ELISA kits were applied to measure the content of reactive oxygen species(ROS)in skin tissue and serum immunoglobulin(IgE),interleukin-17(IL-17)and IL-6,and Western blot was applied to detect the expression of MCP-1 and CC Chemokine receptor 2(CCR2)proteins in skin tissue.Results Compared with the normal group,the depilated skin of the model group developed ulcers,erythema,thickening of the epidermis and spinous layer,and a large number of inflammatory cell infiltration,the scratching times,the number of Mast cells,ROS,IgE,IL-17,IL-6,the protein expression levels of MCP-1 and CCR2 were increased(P＜0.05).Compared with the model group,the erythema,ulcer and inflammatory cell infiltration of skin tissue in the low and high dose Phellodendrine groups were reduced,and no desquamation was found,the scratching times,the number of Mast cells,ROS,IgE,IL-17,IL-6,the protein expression levels of MCP-1 and CCR2 were decreased in turn(P＜0.05).Compared with the high dose Phellodendrine group,the skin erythema,ulcer and inflammatory cell infiltration in the Phellodendrine+MCP-1 group were aggravated,the scratching times,the number of Mast cells,ROS,IgE,IL-17,IL-6,the protein expression levels of MCP-1 and CCR2 were increased(P＜0.05).Conclusion Phellodendrine may reduce the inflammatory response in AD rats by inhibiting MCP-1/CCR2 signaling pathway.
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