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Title: Biochemical mechanism of houttuynia cordata extract on UVB-induced skin inflammation in human keratinocytes
Other Titles: กลไกการออกฤทธิ์เชิงชีวเคมีของสารสกัดจากพลูคาวต่อการอักเสบ ของผิวที่ถูกเหนียวนําด้วยยูวีบีในเซลล์ผิวหนังชนิดเคอราติโนไซต์
Authors: Nattakan Charachit
Authors: Supachai Yodkeeree
Pronngarm Dejkriengkraiku
Nattakan Charachit
Issue Date: Mar-2022
Publisher: Chiang Mai : Graduate School, Chiang Mai University
Abstract: Ultraviolet B (UVB) radiation is not only a major cause of skin photoaging, but also has various harmful effects on human skin, including skin inflammation, cell death, or even skin cancer. Therefore, an effective skin barrier is essential to protect against UVB-induced skin damage. Natural materials have recently attracted the interest of cosmetic researchers due to their therapeutic safety in preventing and protecting the skin from photodamage. In this study, the photoprotective effects of Houttuynia cordata (H. cordata) extract against UVB-induced cell damage were demonstrated in human epidermis keratinocytes (HaCaT cells). First, H. cordata leaves were extracted using a solvent partitioning technique to provide ethanolic (HC-ET), dichloromethane (HC-DM), and ethyl acetate (HC-EA) fractions. The photoprotective effects of H. cordata extract fractions were evaluated using a cell viability assay. The results show that HC-EA attenuated UVB-induced HaCaT cell death, whereas HC-ET and HC-DM had no photoprotective effects. According to the results from HPLC analysis and the photoprotective effects on UVB-induced HaCaT cell death, quercitrin and hyperoside were consequently identified as the major active compounds in HC-EA. Although UVB radiation causes cell apoptosis through intrinsic (mitochondrial) and extrinsic (death receptor-mediated) pathways in many cells. However, UVB primary induces apoptosis via the mitochondrial pathway in human keratinocytes. The results show that HC-EA, quercitrin, and hyperoside showed protective effects against UVB-induced apoptosis through the mitochondrial pathway by attenuating mitochondrial depolarization and the activation of caspase-3, caspase-9, and PARP-1. Moreover, intracellular ROS generated by UVB causes oxidative damage to other biomolecules such as proteins, lipids, and nucleic acids, resulting in oxidative stress. The strong antioxidant activities of HC-EA, quercitrin, and hyperoside were evaluated by ABTS and DPPH assays. Furthermore, HC-EA, quercitrin, and hyperoside exerted photoprotective effects to reduce intracellular ROS generated by UVB in HaCaT cells. HC-EA, quercitrin, and hyperoside also enhanced the antioxidant defense system, including antioxidant enzymes HO-1 and SOD1 via the activation of Nrf2 signaling pathway. Additionally, UVB-induced ROS production causes inflammation by activating signaling pathways that induce the expression of pro-inflammatory cytokines and mediators such as TNF-a, IL-6, IL-8, COX-2, and iNOS. The results demonstrated the anti-inflammatory effects of HC-EA, quercitrin, and hyperoside by attenuating the expression of UVB-induced pro-inflammatory mediators, including IL-6, IL-8, COX-2, and iNOS in HaCaT cells. Finally, the signaling pathways involved in the photoprotective effects of HC-EA, quercitrin, and hyperoside were elucidated. The results show that HC-EA and the compounds enhanced cell protection by activating Nrf2, an important transcription factor that regulates the expression of antioxidant enzymes, and improved cell survival by activating ERK and Akt signaling pathways, as confirmed by cotreatment of HC-EA and the compounds with inhibitors to ERK and Akt, followed by a cell viability assay. On the other hand, HC-EA and the compounds suppressed UVB-induced phosphorylation of JNK and p38 MAPK signaling pathways, which is responsible for their anti-apoptosis and anti-inflammatory effects. Therefore, the evidence summarized shows that HC-EA, quercitrin, and hyperoside reduced UVB-induced photodamage in HaCaT cell via modulating MAPKs, Akt, and Nrf2 signaling pathways.
Appears in Collections:MED: Theses

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