Mechanism of Guomin Decoction(过敏煎)to Improve Atopic Dermatitis by Inhibiting Mast Cell Degranulosis through IgE/FcεRI Pathway
Objective To study the mechanism of Guomin Decoction(过敏煎)in improving atopic dermatitis through in vitro and in vivo experiments.Methods The model of atopic dermatitis(AD)was established by repeated stimulation of 2,4-dinitro-chlorobenzene(DNCB).Loratadine Tablets and Guomin Decoction with low,medium and high doses(1.32,2.64,5.28 g/kg)were administered.The levels of total immunoglobulin E(IgE),interleukin-4(IL-4)and interleukin-13(IL-13)in serum were detected by ELISA.The expression levels of IL-4 and IL-13 in skin lesions were determined by immunohistochemistry(IHC)method.In vitro,anti-DNP-IgE/DNP-HSA was used to induce RBL-2H3 cell replication degranulation model.MTS method was used to detect the activity of Guomin Decoction on RBL-2H3.ELISA was used to detect the β-Hex enzyme release rate and the levels of histamine,leukotriene B4(LTB4),IL-4 and IL-13 in cell supernatant.The mRNA expressions of histamine,IL-4 and IL-13 were detected by reverse transcription-polymerase chain reaction(RT-PCR),and the protein ex-pressions of phosphorylation-extracellular regulated protein kinases(p-ERK)/ERK),phosphorylation-c-Jun N-terminal kinase(p-JNK)/JNK and p-p38/p38 were detected by Western blotting.Results Compared with those of the model group,the levels of total IgE,IL-4 and IL-13 in serum of AD mice in Guomin Decoction groups were significantly decreased(P＜0.05,P＜0.01),and the expressions of IL-4 and IL-13 in skin lesions of AD mice were decreased.β-HEX enzyme release rates(P＜0.05,P＜0.01)and the levels of histamine,LTB4,IL-4 and IL-13(P＜0.05,P＜0.01)were significantly decreased after degranulation of RBL-2H3 cells.The mRNA expressions of histamine,IL-4 and IL-13(P＜0.01)and protein expres-sions of p-ERK/ERK,p-JNK/JNK and p-p38/p38(P＜0.05,P＜0.01)were significantly decreased.Conclusion Guomin Decoction ameliorates atopic dermatitis by regulating Th2 type response and total IgE level in serum,possibly through IgE/FcεRI pathway inhibiting mast cell degranulosis.
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