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HaCaT 세포주에서 나복근 즙 (Juice of Raphanus sativus var)에 의한 아토피 완화 효과에 관한 연구
이승제(Seung-Je Lee),임은경(Eun-Gyeong Lim),김가연(Ga-Yeon Kim),전미지(Mi-Ji Jeon),김상용(Sang-Yong Kim),김영민(Young-Min Kim),유제근(Geun Yoo) 한국생물공학회 2017 KSBB Journal Vol.32 No.4
Raphanus sativus var is widely known as herbs for reducing skin heat and for deciphering internal organs. Also, Raphanus sativus var has various medical effects. But, the effects of atopic treatment of Raphanus sativus var were not investigated. Therefore, we assessed the anti-atopic dermatitis and anti-inflammatory effects of juice of Raphanus sativus var in HaCaT cells. MTT assay showed that the juice of Raphanus sativus var was not cytotoxic effect on the HaCaT cells. The HaCaT cell migration was demonstrated by cells migration assay. TNF-α and IFN-γ induces production of inflammatory cytokines such as CCL17, CCL 27, IL-1β, IL-6 and IL-8 expression. Juice of Raphanus sativus var could inhibit TNF-α and IFN-γ induced mRNA expression levels of CCL17, CCL 27, IL-1β, IL-6 and IL-8 gene. Furthermore, we determined the effects of skin turnover through organotypic cell culture and H&E stain. Our study showed that the treatment of HaCaT cells with the juice of Raphanus sativus var in the observed that its skin recovered to normal condition. These results suggested that the possibility Juice of Raphanus sativus var for prevention and treatment of skin inflammatory diseases such as atopic dermatitis.
Ye Seul Park(박예슬),Gun He Nam(남건희),Kyung Jo Jo(조경조),Hye Won Kawk(곽혜원),Je-Geun Yoo(유제근),Jin Dong Jang(장진동),Sang Moon Kang(강상문),Sang Yong Kim(김상용),Young Min Kim(김영민) 한국생물공학회 2019 KSBB Journal Vol.34 No.3
Collagen is decomposed by MMP-1, an enzyme induced by transcription factor activator protein 1 (AP-1) and matrix metalloproteinase-9 (MMP-9). Action of MMPs in inflammatory response promotes inflammatory cell movement and secretion, resulting in wrinkles on the skin. After using Bacillus sp. fermentation system and water, Artemisia vulgaris was fermented to prepare different solvent fractions using water, dichloromethane, hex ane, n-butanol, and ethyl acetate. These fractions were used to assess their effects on cell survival, wound healing, MMP-1/MMP-9 and procollagen type I C-peptide (PICP) expression, and skin turnover. MTT assay showed that cell viability of each treated group was 103% to 121%, indicating that A. vulgaris fractions were not toxic compared to control (cell viability: 100%). Wound healing assay revealed that wound healing ability in each treated group was 51% to 61%. This was lower than wound healing area in the control. Using RT-PCR, inhibition of MMP-1/MMP-9 gene expression was examined. As a result, each group treated with fraction showed reduced expression of both MMP-1 and MMP-9 compared to tumor necrosis factor-α (TNF-α) treatment group. Effects on collagen biosynthesis were analyzed using a PICP ELISA Kit. The group in which Artemisia vulgaris was treated increased collagen synthesis from 141 to 262ng/mL compared to the control group. Three-dimensional cell culture revealed that each fraction could increase skin wall formation. These results suggest that each fractions has anti-aging and anti-wrinkle effects on the skin, indicating its suitability as a functional material.
Hep3B 간암세포에서 개똥쑥 추출물에 의한 Cell Cycle Arrest 효과
김은지(Eun Ji Kim),김근태(Guen Tae Kim),김보민(Bo Min Kim),임은경(Eun Gyeong Lim),김상용(Sang Yong Kim),하성호(Sung Ho Ha),김영민(Young Min Kim),유제근(Je-Geun Yoo) 한국생물공학회 2015 KSBB Journal Vol.30 No.4
Cells proliferate via repeating process that growth and division. This process is G1, S, G2 and M four phases consists. Monitoring the progression of the cell cycle is a specific step that to be a continuous process is repeated to adjust the start of the next step. At this time, this process is called a Checkpoint. Currently, there are three known checkpoints that G1-S phase, G2-M phase, and the M phase. In this study, we confirmed that cell cycle arrest effects by ethanol extracts of Artemisia annua Linne (AAE) in Hep3B liver cancer cells. AAE was regulated proteins which involved in cell cycle such as pAkt, pMDM2, p53, p21, pCDK2 (T14/Y15). AAE induced cell cycle arrest in G1 checkpoint through phosphorylation of CDK2. Akt and p53 upstream is inhibited by AAE and p53 activated by non-activated pMDM2, p53 inhibitor. Thereby, activated p53 is transcript to p21 and activated p21 protein is combined with Cyclin E-pCDK2 complex. Therefore, we confirmed that AAE-induced cell cycle arrest was occurred by p21-Cyclin E-pCDK2 complex by inhibition of pAkt signal. Because of this cell cycle can’t pass to S phase from G1 phase.