Abstract
In the present study, we investigated the potential of opuntiol, isolated from Opuntia ficus-indica, against UVA radiation-mediated inflammation and skin photoaging in experimental animals. The skin-shaved experimental mouse was subjected to UVA exposure at the dosage of 10 J/cm2 per day for ten consecutive days (cumulative UVA dose: 100 J/cm2). Opuntiol (50 mg/kg b.wt.) was topically applied one hour before each UVA exposure. UVA (100 J/cm2) exposure induces epidermal hyperplasia and collagen disarrangement which leads to the photoaging-associated molecular changes in the mouse skin. Opuntiol pretreatment prevented UVA-linked clinical macroscopic skin lesions and histological changes in the mouse skin. Further, opuntiol prevents UVA-linked dermal collagen fiber loss in the mouse skin. Short-term UVA radiation (100 J/cm2) activates MAPKs through AP-1 and NF-κB p65 transcriptional pathways and subsequently induces the expression of inflammatory proteins and matrix-degrading proteinases in the mouse skin. Interestingly, opuntiol pretreatment inhibited UVA-induced activation of iNOS, VEGF, TNF-α, and COX-2 proteins and consequent activation of MMP-2, MMP-9, and MMP-12 in the mouse skin. Moreover, opuntiol was found to prevent collagen I and III breakdown in UVA radiation-exposed mouse skin. Thus, opuntiol protects mouse skin from UVA radiation-associated photoaging responses through inhibiting inflammatory responses, MAPK activation, and degradation of matrix collagen molecules.
Highlights
The skin is the primary outmost layer of the human body, and it acts as an initial safeguard against harmful effects of environmental and biological factors [1]
We report the preventive effect of opuntiol against UVA radiation-associated photoaging responses in the mouse skin
Monoclonal antibodies such as cyclooxygenase-2 (COX-2), nuclear factor kappa B p65 (NF-κB p65), vascular endothelial growth factor (VEGF), tumor necrotic factor-alpha (TNF-α), interleukin-6 (IL-6), inducible nitric oxide synthase, and anti-mouse and goat antimouse IgG-HRP polyclonal antibodies were acquired from Santa Cruz, USA
Summary
The skin is the primary outmost layer of the human body, and it acts as an initial safeguard against harmful effects of environmental and biological factors [1]. The skin can be possessed with elastic and collagen fibers and proteoglycan-reliant matrices [2]. UVA radiation (320–400 nm) has been considered as aging rays by induction of oxidative stress, mitogen-activated protein kinases (MAPKs), and inflammatory signaling [4]. The environmental UVA radiation-linked photoaging is characterized by degradation of collagen, premature skin aging, wrinkle formation, and erythema of the skin [5]. UVA radiation induces excessive production of reactive oxygen species (ROS) through cellular photosensitizers that lead to the signatures of photoaging and inflammation in the dermal skin layers [6]
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