Protective effect of curcumin against ultraviolet A irradiation‑induced photoaging in human dermal fibroblasts

Abstract

Ultraviolet (UV) radiation induces DNA damage, oxidative stress, and inflammatory processes in skin, resulting in photoaging. Natural botanicals have gained considerable attention due to their beneficial protection against the harmful effects of UV irradiation. The present study aimed to evaluate the ability of curcumin (Cur) to protect human dermal fibroblasts (HDFs) against ultraviolet A (UVA)-induced photoaging. HDFs were treated with 0–10 µM Cur for 2 h and subsequently exposed to various intensities of UVA irradiation. The cell viability and apoptotic rate of HDFs were investigated by MTT and flow cytometry assays, respectively. The effect of UVA and Cur on the formation of reactive oxygen species (ROS), malondialdehyde levels, which are an indicator of ROS, and the levels/activity of antioxidative defense proteins, including glutathione, superoxide dismutase and catalase, were evaluated using 2′,7′-dichlorofluorescin diacetate and commercial assay kits. Furthermore, western blotting was performed to determine the levels of proteins associated with endoplasmic reticulum (ER) stress, the apoptotic pathway, inflammation and the collagen synthesis pathway. The results demonstrated that Cur reduced the accumulation of ROS and restored the activity of antioxidant defense enzymes, indicating that Cur minimized the damage induced by UVA irradiation in HDFs. Furthermore, western blot analysis demonstrated that Cur may attenuate UVA-induced ER stress, inflammation and apoptotic signaling by downregulating the protein expression of glucose-regulated protein 78, C/EBP-homologous protein, nuclear factor-κB and cleaved caspase-3, while upregulating the expression of Bcl-2. Additionally, it was demonstrated that Cur may regulate collagen metabolism by decreasing the protein expression of matrix metalloproteinase (MMP)-1 and MMP-3, and may promote the repair of cells damaged as a result of UVA irradiation through increasing the protein expression of transforming growth factor-β (TGF-β) and Smad2/3, and decreasing the expression of the TGF-β inhibitor, Smad7. In conclusion, the results of the present study indicate the potential benefits of Cur for the protection of HDFs against UVA-induced photoaging and highlight the potential for the application of Cur in skin photoprotection.

Role of PGE-2 and Other Inflammatory Mediators in Skin Aging and Their Inhibition by Topical Natural Anti-Inflammatories

“…A summary of some of this previously unpublished screening data is shown in Table 2. As has been reported by others [173,174], curcumin is perhaps the most potent natural compound available for blocking a wide variety of inflammatory mediators, including PGE-2, and for protecting the skin from photoaging [175,176]. As shown in Table 2, curcumin is able to completely suppress the UVR or TPA mediated increase in PGE-2, IL-1, and TNF-alpha.…”

Ceria Nanoparticles Decrease UVA-Induced Fibroblast Death Through Cell Redox Regulation Leading to Cell Survival, Migration and Proliferation

“…These cells are the major cell type in the dermis and play a pivotal role in skin physiology ( Heather et al, 2018 ) contributing to extracellular-matrix (ECM) and collagen production (maintaining the skin’s structural integrity) and playing an important role in cutaneous wound healing process ( Bainbridge et al, 2013 ). In recent years, numerous studies have been conducted on the role of fibroblasts in wound healing and how this process gets disrupted under UVA radiation ( Heather et al, 2018 ; Liu et al, 2018 ; Chen et al, 2019 ).…”

A Zingerone Analog, Acetyl Zingerone, Bolsters Matrisome Synthesis, Inhibits Matrix Metallopeptidases, and Represses IL-17A Target Gene Expression

“…Similar to Z, the benefits of curcumin for treatment or prevention of skin aging may stem from MMP inhibition (e.g., MMP-1, MMP-2, MMP-3, MMP-9, and MMP-13) (Kumar et al, 2012). Curcumin additionally may confer protection against photoaging by activating antioxidant defenses and reducing endoplasmic reticulum stress and inflammation (Liu et al, 2018).…”