Anti-Inflammatory Effects Exerted by 14-Methoxyalternate C from Antarctic Fungal Strain <i>Pleosporales</i> sp. SF-7343 via the Regulation of NF-κB and JAK2/STAT3 in HaCaT Human Keratinocytes

Atopic dermatitis (AD) is a chronic inflammatory skin disease with a profound negative impact on patients’ quality of life. Four known secondary fungal metabolites were found in the chemical study of the Antarctic fungus <i>Pleosporales</i> sp. SF-7343, including 14-methoxyalternate C (&...

Full description

Bibliographic Details
Main Authors: Linsha Dong, Thao Quyen Cao, Zhiming Liu, Nguyen Quoc Tuan, Youn-Chul Kim, Jae Hak Sohn, Joung Han Yim, Dong-Sung Lee, Hyuncheol Oh
Format: Article
Language:English
Published: MDPI AG 2022-11-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/23/14642
Description
Summary:Atopic dermatitis (AD) is a chronic inflammatory skin disease with a profound negative impact on patients’ quality of life. Four known secondary fungal metabolites were found in the chemical study of the Antarctic fungus <i>Pleosporales</i> sp. SF-7343, including 14-methoxyalternate C (<b>1</b>), 5′-methoxy-6-methyl-biphenyl-3,4,3′-triol (<b>2</b>), 3,8,10-trihydroxy-4-methoxy-6-methylbenzocoumarin (<b>3</b>), and alternariol monomethyl ether (<b>4</b>). Additionally, we identified the skin anti-inflammatory composition from the SF-7343 strain. Interleukin-8 and -6 Screening results showed that compound <b>1</b> inhibited IL-8 and IL-6 in tumor necrosis factor-α/interferon-γ stimulated HaCaT cells. Compound <b>1</b> showed inhibitory effects on MDC and RANTES. It also downregulated the expression of intercellular adhesion molecule-1 (ICAM-1) and upregulated the expression of involucrin. The results of the mechanistic study showed that compound <b>1</b> inhibited the nuclear translocation of nuclear factor-kappa B p65 and STAT3. In conclusion, this study demonstrates the potential of the Antarctic fungal strain SF-7343 as a bioactive resource to inhibit skin inflammation, such as AD.
ISSN:1661-6596
1422-0067