Hyperoside and Quercitrin in Houttuynia cordata Extract Attenuate UVB-Induced Human Keratinocyte Cell Damage and Oxidative Stress via Modulation of MAPKs and Akt Signaling Pathway.

Nattakan Charachit,Supachai Yodkeeree,Amonnat Sukhamwang,Pornngarm Dejkriengkraikul

doi:10.3390/antiox11020221

Abstract

Ultraviolet radiation is a major environmental harmful factor on human skin. In this paper, we investigate the potential mechanism of Houttuynia cordata extract on UVB-induced HaCaT keratinocyte cell death and inflammation. We found that Houttuynia cordata ethyl acetate extract fraction (HC-EA) protected against UVB-induced cell damage. The HPLC results indicate that quercitrin and hyperoside are the major polyphenolics in HC-EA and are responsible for providing protection against UVB-induced cell death. These responses were associated with the regulation of caspase-9 and caspase-3 activation, which rescued HaCaT cells from UVB-induced apoptosis. In addition, HC-EA, quercitrin, and hyperoside attenuated UVB-induced inflammatory mediators, including IL-6, IL-8, COX-2, and iNOS. Furthermore, the treatment of cells with HC-EA and its active compounds abolished intracellular ROS and increased levels of heme oxygenase-1 and superoxide dismutase. UVB-induced ROS production mediated Akt and mitogen activated protein kinases (MAPKs) pathways, including p38, ERK, and JNK. Our results show HC-EA, quercitrin, and hyperoside decreased UVB-induced p38 and JNK phosphorylation, while increasing ERK and Akt phosphorylation. MAPKs and Akt mediated cell survival and death were confirmed by specific inhibitors to Akt and MAPKs. Thus, HC-EA, which contains quercitrin and hyperoside, protected keratinocyte from UVB-induced oxidative damage and inflammation through the modulation of MAPKs and Akt signaling.

Highlights

Ultraviolet B (UVB) exposure is a major extrinsic cause of skin damage, aging, inflammation, tanning, wrinkling, and skin carcinogenesis
We investigated whether Houttuynia cordata ethyl acetate extract fraction (HC-EA), quercitrin, and hyperoside protected HaCaT kerWe investigated whether apoptosis
IN this study, we found that Houttuynia cordata Thunb (HC)-EA, quercitrin, and hyperoside decreased UVB-induced caspase-9 activation, which in part accounts for its protective effect of the UVB-mediated disruption of its mitochondrial membrane potential

Summary

Introduction

Ultraviolet B (UVB) exposure is a major extrinsic cause of skin damage, aging, inflammation, tanning, wrinkling, and skin carcinogenesis. These biological effects are based on electromagnetic energy converted from UVB radiation to molecular oxygen, which in turn generates certain pivotal reactive oxygen species (ROS), such as hydrogen peroxide, superoxide anions, and hydroxyl radicals. UVB can directly induce DNA damage, in particular cyclobutane pyrimidine dimers and 6-4 photo adducts, in human skin cells [1]. The direct DNA damage and ROS production caused by UVB exposure lead to the activation of cytoplasmic signal transduction pathways, which are related to cell survival, death, and inflammation [2]. Well-functioning skin cells employ a protective antioxidant system that involve superoxide dismutase (SOD), catalase, glutathione peroxidase, and heme oxygenase-1 (HO-1) to defend against the destructive effects of ROS [3]

Methods

Results

Conclusion