Ultraviolet B Irradiation Induces Nrf2 Degradation in Human Dermal Fibroblasts

碩士 === 國防醫學院 === 生物化學研究所 === 106 === Dermis is principally made of fibroblasts. In addition to natural aging occurred in all organs, sunlight exposure is a harmful factor to casuse extra damage to dermal fibroblast, particularly the exposure to ultraviolet B irradiation. It induced reactive oxygen s...

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Bibliographic Details
Main Authors: Jhap, Tian-You, 趙天佑
Other Authors: Sheau-Huei Chueh
Format: Others
Language:zh-TW
Published: 2018
Online Access:http://ndltd.ncl.edu.tw/handle/apxng2
Description
Summary:碩士 === 國防醫學院 === 生物化學研究所 === 106 === Dermis is principally made of fibroblasts. In addition to natural aging occurred in all organs, sunlight exposure is a harmful factor to casuse extra damage to dermal fibroblast, particularly the exposure to ultraviolet B irradiation. It induced reactive oxygen species generation that caused damage and apoptosis in the cells. Nrf2 is a transcription factor, and it is also a regulator of ROS. The downstream of Nrf2 including glutathione and heme oxygenase-1 eliminate ROS. The interesting thing UVB caused ROS generation and damaged the cells since Nrf2 is a guard in the cells. How is the homeostasis of Nrf2? In this study, we found that the cell number of human dermal fibroblast and Nrf2 decreased after exposuring UVB 24hr, it also caused ROS generation and enhanced intracellular calcium concentration. 12-HETE is a product after UVB exposure, it also decreased Nrf2 and enhanced intracellular calcium concentration. Baicalein is an inhibitor of 12-lipoxygenase, it could inhibit the phenomenon after UVB exposure. We confirmed the degradation of Nrf2 after exposuring UVB, Nrf2 would trend Calcium-GSK3β-Nrf2 -β-TrCP/Cullin-1.