Hui-Jie Fan1, Ze-Ping Xie2, Zi-Wen Lu3, Zhang-Bin Tan4, Yi-Ming Bi5, Ling-Peng Xie6, Yu-Ting Wu7, Wen-Tong Zhang8, Kevin Liu-Kot9, Bin Liu10, Ying-Chun Zhou11. 1. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 15521107492@163.com. 2. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 326301458@qq.com. 3. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 1148131331@qq.com. 4. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 249880441@qq.com. 5. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 451645244@qq.com. 6. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 845639520@qq.com. 7. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: 1603406288@qq.com. 8. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: zhangwentong.com@qq.com. 9. Department of Biology, Boston University, Boston, MA, 02215, USA. Electronic address: Kliukot@bu.edu. 10. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Cardiology, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong 510260, China. Electronic address: xmhoolv@163.com. 11. School of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Traditional Chinese Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China. Electronic address: zhychun@126.com.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Si-Ni-San (SNS) is a well-known decoction in traditional Chinese medicine. Although studies have indicated that the anti-inflammatory and anti-allergic properties of SNS and its components can account for their therapeutic effects, the role and mechanism of SNS in treating skin dysfunction remain unclear. AIM OF THE STUDY: Atopic dermatitis (AD), a disorder known for its prevalence in infants and adults, severely influences the quality of life of affected patients. In this study, we aimed to investigate the anti-inflammatory and immune response modulations of SNS in 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin dysfunction. MATERIALS AND METHODS: Dermatitis was induced in Kunming mice by the topical application of DNCB. SNS or dexamethasone (positive control) was topically applied every day over the course of the 21-day study. The following were assessed: dermatitis severity scores; ear and dorsal skin haematoxylin and eosin staining; interleukin (IL)- 1α, IL-1β, IL-2, IL-4, IL-6, and tumour necrosis factor (TNF)-α cytokine levels in the serum; spleen index; spleen CD4 + /CD8 + T lymphocyte ratio; and phosphorylation levels of mitogen-activated protein kinases (MAPKs- p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK)), IκB-α, and nuclear factor (NF)-κB (p65) in skin lesions. RESULTS: SNS significantly alleviated the symptoms of AD-like lesions induced by DNCB, decreased the infiltration of inflammatory cells in the ear and dorsal tissues, suppressed the increased cytokine levels in the serum, reduced the CD4 + /CD8 +T lymphocyte ratio in the spleen, and downregulated the activation of MAPKs, IκB-α, and NF-κB (p65) in the dorsal skin. The effects were similar to those of dexamethasone. CONCLUSIONS: SNS alleviated the DNCB-induced AD-like skin dysfunction in mice through anti-inflammatory and immune system modulation, indicating that SNS shows potential for AD treatment in clinical settings.
ETHNOPHARMACOLOGICAL RELEVANCE: Si-Ni-San (SNS) is a well-known decoction in traditional Chinese medicine. Although studies have indicated that the anti-inflammatory and anti-allergic properties of SNS and its components can account for their therapeutic effects, the role and mechanism of SNS in treating skin dysfunction remain unclear. AIM OF THE STUDY: Atopic dermatitis (AD), a disorder known for its prevalence in infants and adults, severely influences the quality of life of affected patients. In this study, we aimed to investigate the anti-inflammatory and immune response modulations of SNS in 2,4-dinitrochlorobenzene (DNCB)-induced AD-like skin dysfunction. MATERIALS AND METHODS:Dermatitis was induced in Kunming mice by the topical application of DNCB. SNS or dexamethasone (positive control) was topically applied every day over the course of the 21-day study. The following were assessed: dermatitis severity scores; ear and dorsal skin haematoxylin and eosin staining; interleukin (IL)- 1α, IL-1β, IL-2, IL-4, IL-6, and tumour necrosis factor (TNF)-α cytokine levels in the serum; spleen index; spleen CD4 + /CD8 + T lymphocyte ratio; and phosphorylation levels of mitogen-activated protein kinases (MAPKs- p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK)), IκB-α, and nuclear factor (NF)-κB (p65) in skin lesions. RESULTS: SNS significantly alleviated the symptoms of AD-like lesions induced by DNCB, decreased the infiltration of inflammatory cells in the ear and dorsal tissues, suppressed the increased cytokine levels in the serum, reduced the CD4 + /CD8 +T lymphocyte ratio in the spleen, and downregulated the activation of MAPKs, IκB-α, and NF-κB (p65) in the dorsal skin. The effects were similar to those of dexamethasone. CONCLUSIONS: SNS alleviated the DNCB-induced AD-like skin dysfunction in mice through anti-inflammatory and immune system modulation, indicating that SNS shows potential for AD treatment in clinical settings.
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