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Evidence-Based Complementary and Alternative Medicine
Volume 2018, Article ID 1096920, 12 pages
Research Article

The Anti-Inflammatory Effect of Fructus Kochiae on Allergic Contact Dermatitis Rats via pERK1/2/TLR4/NF-κB Pathway Activation

1Hunan Provincial Maternal and Child Health Care Hospital, Changsha 410008, China
2College of Biomedical Engineering, South-Central University for Nationalities, Wuhan 430074, China

Correspondence should be addressed to Bo Ouyang; moc.qq@2775940501

Received 4 July 2017; Revised 19 October 2017; Accepted 12 December 2017; Published 4 January 2018

Academic Editor: Jae Youl Cho

Copyright © 2018 Zuoqi Xiao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Allergic contact dermatitis (ACD) is a common irritability skin disease, which can be cured by using the Chinese patent medicine. To explore the pharmacological effect of total flavonoids of Fructus Kochiae (FK) on ACD, we used dinitrochlorobenzene- (DNCB-) induced ACD rats. Five groups were used in our experiments. The normal group and the DNCB group were treated with 0.5% CMC-Na; the DNCB + hFK group was treated with a high dose of total flavonoids of FK (200 mg/kg); the DNCB + lFK group was treated with a low dose of FK (100 mg/kg); the DNCB + Pre group was treated with prednisolone acetate (2.5 mg/kg). The results showed that FK treatment had significantly attenuated the inflammation induced by DNCB. The increased concentration of cytokines including IL-6, IL-18, and IFN-γ in ACD rats could be reversed by the FK administration, while IL-10 expressed the opposite result; the expression level of TLR4, pERK1/2, and NF-κB could be downregulated by the treatment with FK in the ACD rat. In a word, the total flavonoids of the FK had an anti-inflammatory effect on the DNCB-induced ACD rat; this regulatory mechanism was highly possible based on the pERK1/2/TLR4-NF-κB pathway activation.