Abstract
Photodamages caused by UVA radiation induced oxidative injuries are closely related to photoaging and skin cancer. Paeoniflorin (PF), extracted from the root of Paeonia lactiflora, has been reported to be an effective antioxidant. PLIN2, known as adipose differentiation-related protein, has been previously involved in the regulation of oxidative stress. In this study, we were sought to investigate the photo-protective property of PF and PLIN2 in UVA-radiated human dermal fibroblasts (HDFs). HDFs were pre-treated with PF (800 μM) followed by UVA radiation (22.5 J/cm2). MTS activity, cell apoptosis, ROS, MDA, and SOD were detected, respectively. The expressions of Nrf2, HO-1, NQ-O1, and PLIN2 were determined using RT-qPCR or western blot. Nrf2 was silenced by siRNA, and PLIN2 was overexpressed via lentiviral transduction. Comparing to the UVA radiation, PF pre-treatment could prominently increase the MTS activity, decrease cell apoptosis, reduce the generations of ROS and MDA, increase the activity of SOD and increase the expression of Nrf2 and its target genes HO-1 and NQ-O1. When Nrf2 was knocked down, PF lost above protective properties. In addition, UVA induced oxidative stress led to upregulation of PLIN2 and the latter could be decreased by PF. Overexpression of PLIN2 improved MTS activity and reduced MDA level in HDFs. The combination of PLIN2 overexpression and PF pre-treatment corporately inhibited UVA-induced injury. Besides, we also found that PF and PLIN2 had a compensatory protection against UVA induced oxidative stress. In conclusion, our study demonstrated that UVA induced photodamages could be inhibited by PF via Nrf2/HO-1/NQ-O1 signaling pathway or by PLIN2, and the combination of PLIN2 overexpression and PF played additive effects against UVA-related oxidative stress.
Highlights
Ultraviolet A (UVA) radiation (315–400 nm) is a major environmental challenge to the skin (Pinnell, 2003; Bachelor and Bowden, 2004)
Fibroblasts were exposed to different doses of UVA (0, 20, 22.5, 25 J/cm2), and we found that UVA radiation could induce cell injury in a dose-dependent manner (Figure 1B)
Pretreatment of PF and UVA were likely to corporately increase the expressions of these three proteins 12 h after the UVA radiation (Figure 2F). These results have provided evidence of the participation of the nuclear factor erythroid 2-like 2 (Nrf2)/heme oxygenase 1 (HO-1)/NQ-O1 signaling in the protection of human dermal fibroblasts (HDFs) against UVA induced oxidative stress by PF
Summary
Ultraviolet A (UVA) radiation (315–400 nm) is a major environmental challenge to the skin (Pinnell, 2003; Bachelor and Bowden, 2004). Some studies have revealed that UVA generated ROS may cause lipid peroxidation, apoptosis, and upregulation of nuclear factor erythroid 2-like 2 (Nrf2), an oxidative stress marker (Kulms et al, 2002; Hirota et al, 2005; Hseu et al, 2012). Chemical associated oxidative stress has been reported to induce increase in PLIN2 which in turn protected cells against ROS and preserved the mitochondrial integrity in breast cancer cells (Cadenas et al, 2019). We investigated the anti-photodamage potential and the underlying mechanism of PF in HDFs. The expression levels of PLIN2 induced by UVA alone or in combination with PF pre-treatment and the functions of PLIN2 were detected.
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