PMID- 35204104 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20220228 IS - 2076-3921 (Print) IS - 2076-3921 (Electronic) IS - 2076-3921 (Linking) VI - 11 IP - 2 DP - 2022 Jan 24 TI - 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. LID - 10.3390/antiox11020221 [doi] LID - 221 AB - 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. FAU - Charachit, Nattakan AU - Charachit N AD - Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. FAU - Sukhamwang, Amonnat AU - Sukhamwang A AD - Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. FAU - Dejkriengkraikul, Pornngarm AU - Dejkriengkraikul P AUID- ORCID: 0000-0001-8732-8911 AD - Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. AD - Center for Research and Development of Natural Products for Health, Chiang Mai University, Chiang Mai 50200, Thailand. FAU - Yodkeeree, Supachai AU - Yodkeeree S AD - Department of Biochemistry, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand. AD - Center for Research and Development of Natural Products for Health, Chiang Mai University, Chiang Mai 50200, Thailand. LA - eng GR - 162/2563/Faculty of Medicine Research Fund/ GR - 14/2565/the Center for Research and Development of Natural Products for Health/ PT - Journal Article DEP - 20220124 PL - Switzerland TA - Antioxidants (Basel) JT - Antioxidants (Basel, Switzerland) JID - 101668981 PMC - PMC8868276 OTO - NOTNLM OT - HaCaT keratinocyte OT - Houttuynia cordata OT - UVB OT - anti-apoptosis OT - antioxidant COIS- The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, or in the decision to publish the results. EDAT- 2022/02/26 06:00 MHDA- 2022/02/26 06:01 PMCR- 2022/01/24 CRDT- 2022/02/25 01:03 PHST- 2021/12/31 00:00 [received] PHST- 2022/01/17 00:00 [revised] PHST- 2022/01/21 00:00 [accepted] PHST- 2022/02/25 01:03 [entrez] PHST- 2022/02/26 06:00 [pubmed] PHST- 2022/02/26 06:01 [medline] PHST- 2022/01/24 00:00 [pmc-release] AID - antiox11020221 [pii] AID - antioxidants-11-00221 [pii] AID - 10.3390/antiox11020221 [doi] PST - epublish SO - Antioxidants (Basel). 2022 Jan 24;11(2):221. doi: 10.3390/antiox11020221.