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인간모유두세포에서 자외선A에 대한 세포손상에 Ellagic Acid의 세포보호 효과 및 세포보호기전 분석

Analysis of Cell Protective Effects and Mechanisms of Ellagic Acid Against UVA-induced Damages in Human Dermal Papilla Cells

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This study observed change in expression of transcription of genes, p53 and downstream of p53 in HDPCs that were exposed with UVA, researched into the restraining effect of ellagic acid on cell cycle arrest by UVA and the cell activation effect of ellagic acid, hence implemented in order to provide baseline date for future product development of hair and scalp care products using ellagic acid in HDPCs. In this study, it was proven that ellagic acid reduced occurring cell cycle arrest due to UVA on HDPCs. It was proven that a tumor suppressor gene p53 , which was activated upon DNA damage and cell malfunction and was contributed to cell cycle arrest or apoptosis, was increased by UVA, otherwise it was decreased by ellagic acid treatment. It was found that another tumor suppressor gene Gadd45α and 14-3-3σ also were increased by UVA, to the contrary they were decreased by ellagic acid treatment. Both tumor suppressor genes were a factor which would be avail of adjustment to G2/M arrest could generate G2/M arrest and play a role of repairing DNA. Explaining in other words, it was revealed that ellagic acid worked by repairing DNA and decreasing occurring tumor suppressor genes. UVA on HDPCs generated G2 arrest through the course of synthesizing DNA and passing G2 phase and entering M phase and eventually decreasing Cyclin B occurrence. Results from this study indicates that ellagic acid has a protective effect on human dermal papilla cells where UVA damages. Through which, it is expected that understanding of analysis on ellagic acid’s cell reaction, p53 and p53 downstream molecule, G2/M cell cycle arrest will be of avail for supporting further development of scalp and hair products by employing ellagic acid because it can be used as a basic information and a row material for cosmetics.

Abstract

This study observed change in expression of transcription of genes, p53 and downstream of p53 in HDPCs that were exposed with UVA, researched into the restraining effect of ellagic acid on cell cycle arrest by UVA and the cell activation effect of ellagic acid, hence implemented in order to provide baseline date for future product development of hair and scalp care products using ellagic acid in HDPCs. In this study, it was proven that ellagic acid reduced occurring cell cycle arrest due to UVA on HDPCs. It was proven that a tumor suppressor gene p53 , which was activated upon DNA damage and cell malfunction and was contributed to cell cycle arrest or apoptosis, was increased by UVA, otherwise it was decreased by ellagic acid treatment. It was found that another tumor suppressor gene Gadd45α and 14-3-3σ also were increased by UVA, to the contrary they were decreased by ellagic acid treatment. Both tumor suppressor genes were a factor which would be avail of adjustment to G2/M arrest could generate G2/M arrest and play a role of repairing DNA. Explaining in other words, it was revealed that ellagic acid worked by repairing DNA and decreasing occurring tumor suppressor genes. UVA on HDPCs generated G2 arrest through the course of synthesizing DNA and passing G2 phase and entering M phase and eventually decreasing Cyclin B occurrence. Results from this study indicates that ellagic acid has a protective effect on human dermal papilla cells where UVA damages. Through which, it is expected that understanding of analysis on ellagic acid’s cell reaction, p53 and p53 downstream molecule, G2/M cell cycle arrest will be of avail for supporting further development of scalp and hair products by employing ellagic acid because it can be used as a basic information and a row material for cosmetics.

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