Abstract
Reactive oxygen species (ROS) are a major causative factor of inflammatory responses and extracellular matrix degradation. ROS also cause skin aging and diverse cutaneous lesions. Therefore, antioxidants that inhibit the generation of ROS may be beneficial in the relief of skin aging and diseases. We investigated the anti-skin aging effect of anthraquinones from cultures of Colletotrichum sp., an endophytic fungus isolated from Morus alba L. using human dermal fibroblasts (HDFs). We preferentially evaluated the preventive effects of anti-oxidative anthraquinones (1, 4) against the generation of ROS, nitric oxide (NO), and prostaglandins-E2 (PGE2). Among them, 1,3-dihydroxy-2,8-dimethoxy-6-methylanthraquinone (1) suppressed the generation of ROS, NO, and PGE2 in tumor necrosis factor-alpha (TNF-α)-stimulated HDFs. Compound 1 reversed the TNF-induced increase in matrix metalloproteinase (MMP)-1 and a decrease in procollagen I α1 (COLIA1). It also suppressed inducible NO synthase, cyclooxygenase-2, interleukin (IL)-1β, IL-6, and IL-8, which upregulate inflammatory reactions. Mechanistically, compound 1 suppressed nuclear factor-κB, activator protein 1, and mitogen-activated protein kinases in TNF-α-stimulated HDFs. These results suggest that compound 1 may be beneficial for improving skin aging and diverse cutaneous lesions.
Highlights
The skin is the primary protective organ of the human exodermal system and is in direct contact with potentially harmful factors
We investigated the prevent effect against skin damages of anthraquinones obtained from Colletotrichum sp. using human dermal fibroblasts (HDFs) to identify potential candidates
The compound was the most potent of the four. It prevented the generation of reactive oxygen species (ROS), intracellular calcium ion levels, and phosphorylation of mitogen-activated protein kinases (MAPKs) in glutamatemediated apoptosis [38]
Summary
The skin is the primary protective organ of the human exodermal system and is in direct contact with potentially harmful factors. Antioxidants that inhibit the generation of ROS and MMP-1 may potentially be beneficial in skin aging. The light can directly or indirectly induce several proinflammatory mediators that include prostaglandin E2 (PGE2 ), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL8 [17,18,19] These inflammatory responses are associated with damage to skin fibroblasts, which accelerates the UV irradiation-induced photoaging process [17,20]. The foregoing indicates that anthraquinones should prevent oxidative stress related damage to the skin ECM. We describe the prevent effect of skin damages of anti-oxidative anthraquinones and verify the mechanism of the active compound for TNF-α-stimulated HDFs. 2. USA), skin damages of anti-oxidative anthraquinones and verify the mechanism of the active. The cells were seeded in each size well plate at a density of 3 × 104 cells/cm and
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