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Int Immunopharmacol. 2017 Apr;45:174-179. doi: 10.1016/j.intimp.2017.02.014.

Mangiferin antagonizes TNF-α-mediated inflammatory reaction and protects against dermatitis in a mice model.

Author information

1
Department of Orthopaedics, Qilu Hospital, Shandong University, Jinan, Shandong 250012, PR China.
2
School of Medcine, Shandong University, Jinan, Shandong 250012, PR China.
3
Department of Gynaecology and Obstetrics, Jinan Central Hospital, Shandong University, Jinan, Shandong, 250012, PR China.
4
Department of Pathology, Qilu Hospital, Shandong University, Jinan, Shandong, 250012, PR China. Electronic address: miraculously2008@163.com.

Abstract

This study aimed to investigate whether mangiferin played a protective role in a well-established dermatitis mouse model and tumor necrosis factor alpha (TNF-α)-induced RAW264.7 macrophages. Contact dermatitis is an inflammatory skin disease in the clinic, while its underlying mechanism still remains to be elucidated. Mangiferin, 1,3,6,7-tetrahydroxyxanthone-C2-β-d-glucoside (C-glucosyl xanthone), a natural antioxidant that was reported to inhibit inflammatory reactions, has been recently proved to be a potential therapy for inflammation. As a result, the oxazolone-induced dermatitis mice models were established to explore whether mangiferin has an anti-inflammatory role in vivo. The phosphate-buffered saline treatment groups showed emblematic skin inflammation, whereas the administration of mangiferin obviously inhibited dermatitis in the mice models. Furthermore, exogenous mangiferin alleviated the inflammatory reaction in TNF-α-induced macrophages by suppressing the production of inflammation- and oxidative stress-associated molecules. Also, mangiferin treatment repressed the activation of nuclear factor-kappaB signaling pathway. To sum up, mangiferin could provide a new target for the therapy and prevention of skin inflammation.

KEYWORDS:

Dermatitis; Inflammation; Mangiferin; NF-κB signaling pathway; RAW264.7 macrophage; TNF-α

PMID:
28222357
DOI:
10.1016/j.intimp.2017.02.014
[Indexed for MEDLINE]

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