Photoprotective and immunoregulatory capacity of ginsenoside Rg1 in chronic ultraviolet B-irradiated BALB/c mouse skin

Abstract

The aim of this study was to investigate the photoprotective and immunoregulatory capacities of ginsenoside Rg1 in skin irradiated by chronic ultraviolet B (UVB) and to verify the potential mechanisms of action. BALB/c mice were pretreated with a topical application of ginsenoside Rg1 and irradiated with different doses of UVB daily for 30 consecutive days. Following chronic UVB irradiation, there were significant pathological changes in the skin of the BALB/c mice, including hyperkeratosis, acanthosis, sponge-like edematization and sunburn occurring in the epidermis, while edema, telangiectasis and inflammatory cell infiltration were observed in the papillary layer of the dermis. Treatment with ginsenoside Rg1 was able to reduce such changes induced by UVB irradiation. The number of p53 protein-positive stained cells following UVB irradiation was also observed by immunohistochemical analysis. Ginsenoside Rg1 downregulated the p53 protein expression induced by UVB irradiation, leading to reductions of 69.50, 23.53 and 12.93% at doses of 30, 60 and 120 mJ/cm2, respectively. Using reverse transcription polymerase chain reaction (RT-PCR), reductions in the levels of interferon (IFN)-γ mRNA expression were detected following UVB exposure; reductions of 19.6, 36.3 and 39.6% were observed following UVB irradiation at doses of 30, 60 and 120 mJ/cm2, respectively. The interleukin (IL)-10 mRNA expression levels increased by 40.1, 71.0 and 89.4% and the tumor necrosis factor (TNF)-α mRNA expression levels increased by 36.4, 18.4 and 8.6% following UVB irradiation at doses of 30, 60 and 120 mJ/cm2, respectively. However, pretreatment with ginsenoside Rg1 was observed to markedly attenuate the UVB irradiation-induced effects on the mRNA expression levels of the three cytokines. The topical application of ginsenoside Rg1 was able to protect the irradiated skin from UVB injury and reduce UVB-induced p53 protein expression. Ginsenoside Rg1 also demonstrated a potential regulatory effect on the UVB-induced local expression of the mRNA of the cytokines IFN-γ, IL-10 and TNF-α, which may be important in its immunoregulatory and inflammatory mechanisms.

Naringenin Inhibits UVB Irradiation-Induced Inflammation and Oxidative Stress in the Skin of Hairless Mice

“…Supporting our results, naringenin treatment reduces the TNF-α, IL-1β, and IL-6 levels in an ulcerative colitis model in rats, IFN-γ production in an atopic dermatitis mouse model, Th2 cytokine production (IL-4, IL-5, IL-13) in a murine allergic asthma model, IL-17 levels in murine colitis, IL-23 levels in a human osteoclastogenesis model, TNF-α, IL-1β, IL-6, and IL-10 levels in Chlamydia trachomatis -induced inflammation, and TGF-β expression in nephrotoxicity in mice . The release of these cytokines plays a central role in the recruitment and activation of inflammatory cells, leading to skin damage after UVB exposure. ,,,, Moreover, the inhibition of these cytokines is considered a therapeutic approach to control skin cancer progression and metastasis, psoriasis, contact dermatitis, and other diseases. ,,,− It is likely that the inhibition of cytokine production by naringenin might be related to the inhibition of early inflammatory events such as inhibition of production or effects of ROS and NF-κB activation.…”

“…Activation of the NF-κB pathway by UVB irradiation contributes to skin damage, photoaging, and skin tumor formation . Furthermore, UVB irradiation induces the production of multiple cytokines, including TNF-α, ,, IL-1β, , IL-6, , interferon gamma (IFN-γ), , IL-12, IL-4, IL-5, IL-17, IL-23, IL-10, , and transforming growth factor beta (TGF-β) …”

“…6 Activation of the NF-κB pathway by UVB irradiation contributes to skin damage, photoaging, and skin tumor formation. 6 Furthermore, UVB irradiation induces the production of multiple cytokines, including TNF-α, 6,41,42 IL-1β, 15,43 IL-6, 6,13 interferon gamma (IFN-γ), 41,44 IL-12, 44 IL-4, 41 IL-5, 41 IL-17, 44 IL-23, 44 IL-10, 41,42 and transforming growth factor beta (TGF-β). 13 Pro-inflammatory cytokines (e.g., TNF-α, IL-1β, and IL-6) initiate the cascade of inflammatory events by inducing chemokine release from resident alarm cells and by upregulating adhesion molecules required for transendothelial trafficking of immune cells responsible for boosting the inflammatory response.…”

Regulatory effect of Bcl-2 in ultraviolet radiation-induced apoptosis of the mouse crystalline lens

“…In this respect, Bcl-2 has a positive significance in maintaining cellular 'metabolism'. However, excessive UV radiation or the repeated accumulation of small doses of UV radiation may lead to extensive apoptosis and further induce the occurrence of cataracts (26,27). Therefore, the role of Bcl-2 in apoptosis appears to be a contradictory with negative and positive aspects.…”

20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, a metabolite of ginsenoside Rb1, enhances the production of hyaluronic acid through the activation of ERK and Akt mediated by Src tyrosin kinase in human keratinocytes

“…1A) by gastric fluids and the intestinal microflora (1). Previous studies have demonstrated the beneficial effects of ginsenosides and their metabolites on skin health, such as their wound healing (2,3) and anti-aging effects (4,5), as well as protective effects against untraviolet irradiation (6)(7)(8). Pharmacologically, 20GPPD has anti-inflammatory properties (9), anti-aging effects and promotes skin wound healing (5,10).…”