Perilla frutescens Extracts Enhance DNA Repair Response in UVB Damaged HaCaT Cells.

Eunmi Park,Hyuna Lee

doi:10.3390/nu13041263

Abstract

Physiological processes in skin are associated with exposure to UV light and are essential for skin maintenance and regeneration. Here, we investigated whether the leaf and callus extracts of Perilla frutescens (Perilla), a well-known Asian herb, affect DNA damage response and repair in skin and keratinocytes exposed to Untraviolet B (UVB) light. First, we examined the protective effects of Perilla leaf extracts in UVB damaged mouse skin in vivo. Second, we cultured calluses using plant tissue culture technology, from Perilla leaf explant and then examined the effects of the leaf and callus extracts of Perilla on UVB exposed keratinocytes. HaCaT cells treated with leaf and callus Perilla extracts exhibited antioxidant activities, smaller DNA fragment tails, and enhanced colony formation after UVB exposure. Interestingly, keratinocytes treated with the leaf and callus extracts of Perilla showed G1/S cell cycle arrest, reduced protein levels of cyclin D1, Cyclin Dependent Kinase 6 (CDK6), and γH2AX, and enhanced levels of phosphorylated checkpoint kinase 1 (pCHK1) following UVB exposure. These observations suggest that the leaf and callus extracts of Perilla are candidate nutraceuticals for the prevention of keratinocyte aging.

Highlights

Skin is primarily composed of epidermis and dermis and exposed to a variety of environmental factors including UV radiation
We found that 0.1 μg/mL of Perilla callus extract decreased the proportion of cells in the S phase as compared with DMSO treatment after UV exposure
It has been reported that UV-induced damage increases the levels of pCHK1protein expression during DNA damage and repair response [5,20]

Summary

Introduction

Skin is primarily composed of epidermis and dermis and exposed to a variety of environmental factors including UV radiation. UV exposure is a major factor of age-related changes such as pigmentary changes, thinning, wrinkling, and skin cancer development [1]. Exposure to UVB causes inflammation and immune changes that induce cellular senescence, direct DNA damage, and increases levels of oxidative stress, which can indirectly induce DNA mutagenesis. In response to DNA damage, the DNA response and repair pathway is activated in keratinocytes [3,4]. DNA damage in keratinocytes may result in the accumulation of mutations that prompt cell cycle arrest and promote skin aging. When exposed to UVB, phosphorylated checkpoint kinase 1 (pCHK1) is activated, this causes

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