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

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.

Limonene protects human skin keratinocytes against UVB‐induced photodamage and photoaging by activating the Nrf2‐dependent antioxidant defense system

“…Thus, we suggest that the activation of Nrf2 by limonene is a JNK/SAPK‐ and AKT‐dependent mechanism. A previous study also suggested that exposure of HaCaT cells to dietary phytochemicals, such as hyperoside and quercitrin promote Nrf2 accompanied by the activation of JNK/SAPK and AKT 35 . Based on our results, limonene promoted Nrf2 activation and induction of antioxidant regulators, which were critical protective molecules for the skin against UVB‐induced photodamage.…”

“Biqi” Bayberry Extract Promotes Skeletal Muscle Fiber Type Remodeling by Increasing Fast Myofiber Formation via the Akt/FoxO1 Pathway in Mice

“…Myricetin was also reported to regulate Akt signaling for improving skeletal muscle function in fructose-fed rats [ 36 ]. Hyperoside was found to affect Akt signaling for exerting effects in vivo and in vitro [ 37 , 38 ]. The positive effect of BBE on the Akt-FoxO1 pathway may be attributed to the presences of myricitrin, myricetin, and hyperoside.…”

Effect of transcutaneous neuromodulation on normalization of dermal body temperature and pain in a tender scar in the presence of low back pain: An update and case report

“…Ultraviolet B rays produce electromagnetic energy. 32 Epidermal cells are modulated by UV electromagnetic waves, and although each one has a function, they share a communication network. 10 , 13 This modulates cutaneous sensory transduction, 33 influencing both inflammatory responses and the immune and endocrine systems as a whole.…”