Prevention by the Natural Artocarpin of Morphological and Biochemical Alterations on UVB-Induced HaCaT Cells.

Kunlathida Luangpraditkun,Jarupa Viyoch,Anupong Joompang,Céline Viennet,Pensri Charoensit,Marion Tissot,François Grandmottet,Alin Ciobica

doi:10.1155/2021/5067957

Kunlathida Luangpraditkun, Jarupa Viyoch + Show 6 more

Open Access

https://doi.org/10.1155/2021/5067957

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Abstract

Natural substances have gained considerable attention for skin protection against UV light reactions. Artocarpus altilis plant's heartwood extract is comprised of artocarpin as a major substance, already known for its interesting biological attributes as an antimicrobial, an anti-inflammatory, an antioxidant, and a melanogenesis inhibitor. The present work clarified the mechanism of natural artocarpin (NAR) with a purity of approximately 99% against the effects of UVB-induced HaCaT keratinocyte apoptosis. The indicated results showed that NAR suppresses free radical production (ROS and nitrite) and apoptosis-related molecule activation (caspase-3, p-p53, p-p38, and NF-κB p65) and secretion (TNF-α). Additionally, NAR prevented structural damages (nuclei condensation and fragmentation, apoptotic body formation, impaired cell adherence and round cell shape, disruption of F-actin filament, and clustering of cell death receptor CD95/Fas) and biophysical changes (plasma membrane rigidification). Thus, NAR acts directly from scavenging free radicals generated by UV and indirectly by suppressing morphological and biochemical UV-induced cell damages. Its biological effects are mainly attributed to antioxidant and antiapoptotic properties. Taken together, NAR could be considered as an effective natural product for photoprotective formulations.

Highlights

Keratinocytes (KCs) are the predominant cells in the epidermis, the outermost skin layer
ultraviolet B (UVB)-provoked oxidative stress results in the stimulation of nuclear factor-κB (NF-κB) by p38/mitogen-activated protein kinase (MAPK) relating to cell death, matrix metalloprotease (MMPs) expression, and proinflammatory cytokine release including tumor necrosis factor-alpha (TNF-α) [17, 18]
We studied oxidative stress (ROS and nitric oxide (NO)), biophysical change in the plasma membrane, cell structural features, and expression of apoptosis-related molecules

Summary

Introduction

Keratinocytes (KCs) are the predominant cells in the epidermis, the outermost skin layer. KCs are important cellular targets for solar ultraviolet B (UVB) radiation that is responsible for sunburn, photoaging, immune suppression, and skin cancers [4,5,6,7]. At the cellular and molecular levels, excessive UVB exposure leads to several signaling responses involving morphological and biochemical changes on KCs [8]. Lipid peroxidation leads to Oxidative Medicine and Cellular Longevity changes in the integrity, permeability, and fluidity of the plasma membrane [15]. UVB-provoked oxidative stress results in the stimulation of NF-κB by p38/MAPK relating to cell death, matrix metalloprotease (MMPs) expression, and proinflammatory cytokine release including tumor necrosis factor-alpha (TNF-α) [17, 18]

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