Abstract
Ultraviolet radiation is an environmental carcinogenic agent that enhances inflammation and immunological reactions in the exposed human skin cells leading to oxidative photoaging of the epidermal and dermal segment. In the present study, we investigated the protective role of ursolic acid (UA) against ultraviolet B (UVB) radiation- induced photoaging an in vitro model of human skin dermal fibroblasts. UA-pretreated human skin dermal fibroblast (HDF) cells were exposed to UVB radiation to evaluated cell viability, reactive oxygen species (ROS), mitochondrial membrane potential, lipid peroxidation, antioxidant status, DNA damage, proinflammatory response, apoptotic induction, and matrix metalloproteinase (MMP) alteration. The UA pretreatment of HDFs mitigated the UVB irradiation-induced cytotoxicity, ROS generation, and mitochondrial membrane potential alteration and lipid peroxidation, depletion of antioxidant status, DNA damage, and apoptotic induction. UA pretreatment of HDFs also attenuated the UVB-induced expression of inflammatory (TNF-α and NF-κB) and apoptotic (p53, Bax, and caspase-3) and MMPs (MMP-2 and MMP-9) and enhanced the Bcl-2 protein levels in 20 μM UA treatment, when compared to concentrations. Hence, these results revealed that UA has the potential to mitigate UVB-induced extracellular damage by interfering with the ROS-mediated apoptotic induction and photoaging senescence and thus is a potential therapeutic agent to protect the skin against UVB-irradiation induced photooxidative damage.
Highlights
Ultraviolet radiation, predominantly ultraviolet B (UVB) (290–320 nm wavelength), can be hazardous to human health by inducing cyclobutane pyrimidine dimer (CPD) formation, cellular damage, inflammation, and tissue photodamage [1]
The DNA was not affected in control and human skin dermal fibroblast (HDF) treated with ursolic acid (UA) 20 μM (Figures 6(a) and 6(b)), whereas the DNA was damaged in HDFs treated with UVB 40 mJ/cm2 compared to control (Figure 6(c))
The UA 10 μM+UVB and UA 40 μM+UVB induced moderated apoptotic morphological changes in the HDFs (Figures 7(d) and 7(f)) whereas no apoptosis was observed in HDFs treated with UA 20 μM+UVB (Figure 7(e))
Summary
Ultraviolet radiation, predominantly UVB (290–320 nm wavelength), can be hazardous to human health by inducing cyclobutane pyrimidine dimer (CPD) formation, cellular damage, inflammation, and tissue photodamage [1]. The increased ROS load can mitigate intracellular organelles to cause oxidative damage to cellular proteins, lipids, and DNA This leads to photooxidative damage and the activation of apoptotic signal transduction stimulus that can promote photoaging and skin carcinogenesis. UVB irradiation leads to changes in the elasticcollagenous tissues of the skin by breaking down the core collagen fibrils, a major component of the extracellular matrix [9, 10] These alterations in the extracellular matrix are possibly mediated by MMPs that are known to cause premature wrinkling and aged skin [11]. Since artificial sunscreen agents may generate free radicals themselves when activated by UV light and only few of them can provide full spectral protection against ultraviolet radiation, the use of formulations containing plant-derived antioxidants may have highly beneficial effects for the prevention of skin photoaging. We investigated the protective effect of UA against UVB irradiation-induced oxidative stress-mediated activation of inflammatory response and apoptotic signaling cascades triggering the photoaging in HDFs in vitro
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