Panax ginseng C. A. Meyer Phenolic Acid Extract Alleviates Ultraviolet B-Irradiation-Induced Photoaging in a Hairless Mouse Skin Photodamage Model.

Zhenzhuo Li,Jianzeng Liu,Xiaohao Xu,Daqing Zhao,Rui Jiang,Liwei Sun,Weicheng Hu

doi:10.1155/2021/9962007

Abstract

Here, we evaluated the in vivo skin-protective effects of topical applications of Panax ginseng C. A. Meyer extract (PG2) and its phenolic acid- (PA-) based components against UVB-induced skin photoaging. PG2 or PA applied to skin of hairless mice after UVB-irradiation alleviated UVB-induced effects observed in untreated skin, such as increased transepidermal water loss (TEWL), increased epidermal thickness, and decreased stratum corneum water content without affecting body weight. Moreover, PG2 and PA treatments countered reduced mRNA-level expression of genes encoding filaggrin (FLG), transglutaminase-1 (TGM1), and hyaluronan synthases (HAS1, HAS2, and HAS3) caused by UVB exposure and reduced UVB-induced collagen fiber degradation by inhibiting the expression of matrix metalloproteinase genes encoding MMP-1, MMP-2, and MMP-9. Meanwhile, topical treatments reduced cyclooxygenase-2 (COX-2) mRNA-level expression in photodamaged skin, leading to the inhibition of interleukin-1β (IL-1β) and interleukin-6 (IL-6) mRNA-level expression. Thus, ginseng phenolic acid-based preparations have potential value as topical treatments to protect skin against UVB-induced photoaging.

Highlights

In the human body, the skin is the largest organ
Due to the known antioxidant activities of phenolic acid compounds, here we evaluated PG2 and its main phenolic acid constituents to investigate their abilities to repair skin barrier damage, improve skin hydration, and alleviate matrix metalloproteinases (MMPs)- and inflammation-associated skin photoaging in a UVB-irradiated hairless mouse skin photodamage model
The remaining dried extracts were dissolved in distilled water; equal volumes of three solvents were added in succession to generate separate chloroform, ethyl acetate, and n-butanol extracts. e ethyl acetatederived extract described in this work, designated PG2, was characterized using two methods: high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC-MS) [20, 21]

Summary

Introduction

High-level UV irradiation, especially within the UVB wavelength range, is currently the most frequent cause of skin photodamage. Skin photodamage manifests as epidermal thickening accompanied by increased skin surface dryness, roughness, pigmentation irregularities, solar erythema, transepidermal water loss (TEWL), decreased elasticity, deep wrinkles, and other signs associated with premature aging [3,4,5]. Previous studies have demonstrated that visually apparent signs of UVB-induced skin damage result from irradiation-associated effects that trigger skin barrier dysfunction, skin dehydration, inflammation, and collagen degradation. When the body is exposed to UVB radiation, the skin barrier becomes compromised, resulting in decreased expression of filaggrin (FLG) protein and epidermal damage [6]. FLG, a key regulator of stratum corneum barrier function, undergoes cross-linking with transglutaminase-1

Methods

Results

Conclusion