Abstract
Administration of antioxidants and anti-inflammatory agents is an effective strategy for preventing ultraviolet (UV) irradiation-induced skin damage. Artocarpus communis possesses several pharmacological activities, such as antioxidant, anticancer and anti-inflammation. However, the photoprotective activity of methanol extract of A. communis heartwood (ACM) in ultraviolet irradiation-induced skin damage has not yet been investigated. The present study was performed using ultraviolet absorption, histopathological observation, antioxidant and anti-inflammation assays to elucidate the mechanism of the photoprotective activity of ACM. Our results indicated that ACM displayed a UVA and UVB absorption effect and then effectively decreased scaly skin, epidermis thickness and sunburn cells during ultraviolet irradiation in hairless mice. ACM not only decreased ultraviolet irradiation-mediated oxidative stress, including lowering the overproduction of reactive oxygen species and lipid peroxidation (p < 0.05), but also reduced the levels of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin 1β. Additionally, ACM can decrease the synthesis of cytosolic phospholipase A2, cyclooxygenase, inducible nitric oxide synthase and vascular cell adhesion molecular-1 via inhibiting TNF-α-independent pathways (p < 0.05) in UVB-mediated inflammation and formation of sunburn cells. Consequently, we concluded that ACM extract has a photoprotective effect against UVB-induced oxidative stress and inflammation due to its sunscreen property, and its topical formulations may be developed as therapeutic and/or cosmetic products in further studies.
Highlights
Overproduction of reactive oxygen species (ROS) is an inducible factor caused by the overexpression of pro-inflammatory cytokine during chronic UVB irradiation, such as tumor necrosis factor-α (TNF-α) and interleukin 1, which triggered the expression of cytosolic phospholipase A2 and cyclooxygenase (COX-2), leading to an increase of the prostaglandin level, the formation of sunburn cells and inflammatory cell infiltration and activation [9,10,11]
It is well known that chronic UV irradiation can induce skin damage with a number of pathological changes, including DNA damage [1,2], formation of sunburn cells [23], oxidative stress induction by ROS overproduction [8] and over release of proinflammatory cytokines [24]
The methanol extract of A. communis was observed to exhibit a photoprotective effect, as demonstrated by decreasing epidermis thickness and formation of sunburn cells in hairless mice induced with UVB irradiation
Summary
Overexposure of the skin to ultraviolet (UV) radiation has been shown to induce several pathological changes in skin damage, including erythema, scaling, edema, hyperpigmentation, skin thickness, sunburn cells (apoptotic keratinocyte), immunosuppression, tumorigenesis and aging [1,2,3,4]. TNF-α activates the expression of inducible nitric oxide synthase (iNOS) and vascular cell adhesion molecular-1 (VCAM-1) in UVB-induced skin damaged hairless mice, leading to inflammation progression [12,13]. Antioxidant supplements have been shown to attenuate inflammation and cell death through decreasing oxidative stress, such as traditional medicines [14] and natural products [15]. The aim of the present study was to investigate the photoprotective effects of the methanol extract of A. communis on UVB-induced photodamage in a hairless mice model. We performed the morphological and histopathological examinations, antioxidant activity and anti-inflammation assays to evaluate the photoprotective effects of A. communis in UVB-induced skin damaged hairless mice
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