Protective Effects of Pyridoxamine and Baicalin Against UVC-induced Cell Injury in HaCaT Cells

• Main Authors: WANG,SHOU-CHENG, 王守正
• Other Authors: LIN,SONG-SHEI
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/49844943262791561178

博士 === 中臺科技大學 === 醫學影像暨放射科學系暨研究所 === 104 === Long-term exposure to solar ultraviolet (UV) radiation can cause multiple skin disorders, including skin cancer. Protection against UV-induced damage is, therefore, a worldwide concern. Pyridoxamine, a natural form of vitamin B6, has a potential radio-protection effect for guarding normal epithelial cells from ionizing radiation. Baicalin, a major component of traditional Chinese medicine Scutellaria baicalensis, has been reported to have antioxidant and cytostatic effects on normal epithelial and normal peripheral blood and myeloid cells. In the following study, we examined whether pyridoxamine and baicalin could effectively protect human keratinocytes from damaging short-wave UVC irradiation. UVC-induced programmed cell death in HaCaT cells was abrogated by treated the cells immediately after UVC irradiation with 40, 80 and 160 μM of pyridoxamine. Monitoring the UVC-induced-specific reactive oxygen species, we found that 20, 40, 80 and 160 μM of pyridoxamine was also effective in suppressing the induction of reactive oxygen species by UVC. Baicalin-scavenged reactive oxygen species increased within 2 h after UVC radiation. Baicalin also abrogated UVC-induced apoptosis. In addition, we identified the major products after UVC radiation with T4 UV endonuclease, finding that baicalin prevented cyclobutane pyrimidine dimer formation induced by UVC. Furthermore, baicalin also prevented formation of oxidative adducts induced by UVC. Overall, our results provided evidence showing that pyridoxamine and baicalin were effective in protecting HaCaT cells from UVC-induced programmed cell death and may be a potential anti-UVC agent in life and clinical practice. Key words：pyridoxamine, baicalin, HaCaT cell, UVC, apoptosis, reactive oxygen species, cyclobutane pyrimidine dimers