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C57BL/6 마우스에서 기능성 샴푸 Bonogen의 양모 촉진 효과
홍진태(Jin-Tae Hong),이세라(Se-Ra Lee),김환희(Hwan Hee Kim),조영광(Young-Kwang Jo),백인정(In-Jeoung Baek),연정민(Jung-Min Yon),남상섭(Sang-Seop Nahm),곽동훈(Dong Hoon Kwack),이정은(Jung Eun Lee),이범준(Beom-Jun Lee),윤영원(Young-Won 한국독성학회 2006 Toxicological Research Vol.22 No.3
Bonogen shampoo is composed of several plant extracts which are known to be used in oriental medicine. This study was carried out to investigate the effects of Bonogen shampoo on hair growth in an alopecia model of C57BL/6 mice. There were eight male and female experimental groups including distilled water (DW; negative control), a commercial shampoo [M], 3% minoxidil (MXD) and Bonogen shampoo (BNG). Dorsal skin hair of six-week-old mice was trimmed with an electric clipper carefully not to damage the skin. The next day, mice without skin scratch were selected, randomized and separated in 10 mice per group. The test compounds were topically treated with 0.15 ml per mouse on dorsal skin for 21 days daily and then washed thoroughly with DW. The hair regrowth was determined photographically at 0, 4, 7, 10, 15, 18, and 21 days and histologically at day 21. No clinical signs were observed in all mice. Although body weight was slightly increased in 3% MXD group than other groups, it was not significant. Hair regrowth began to be promoted after 14 days and appeared a distinct regrowth pattern in all animals by topical treatment of test compounds at 18 days. In particular, the topical treatment of bonogen shampoo or 3% MXD for 21 days to dorsal skin accelerated hair regrowth faster than DW or M shampoo. At 21 days, the hair regrowth promotion speed was in order of 3% MXD > BNG > M > DW. The bonogen shampoo or 3% MXD also promoted hair follicle elongation compared to the negative control. These results suggest that bonogen shampoo has hair growth promoting activities and may be useful for treatment of bald or alopecia.
흰쥐 배양 전배자 및 중뇌세포에서 Ochratoxin A의 독성
홍진태(Jin Tae Hong),박귀례(Kui Lea Park),한순영(Soon Young Han),박기숙(Ki Sook Park),김형식(Hyung Sik Kim),오세동(Se Dong Oh),박희정(Hee Jung Park),이이다(Rhee Da Lee),장성재(Seung Jae Jang) 대한약학회 1998 약학회지 Vol.42 No.3
Effects of ochratoxin A (OTA) on embryo development were studied in cultured whole embryos from 9.5 day gestation rat for 48 h. OTA (more than 0.5mcg/ml) induced microcephaly in the cultured rat whole embryos. Protein and DNA content, and DNA synthesis were significantly inhibited by OTA. We next examined whether the microcephaly seen in cultured whole embryo partially results from inhibition of differentiation of embryonic midbrain cells. Embryonic midbrain cells were extracted from 12 day gestation rat embryos, and cultured for 96 hr. OTA ibhibited cell differentiation about 50% over control. We also tested whether OTA-induced embryotoxicity would be associated with oxidative damages. We measured the gamma-glutamyltranspeptidase (gamma-GT) and glutathione peroxidase (GPX) activities, and glutathione (GSH) content in both cultured whole embryos and embryonic midbrain cells. OTA decreased GSH content, whereas slightly increased gamma-GT activity, but GPX activity was not significantly changed. These results show that OTA caused the microcephaly and its effect may be partially due to the inhibition of cell differentiation of embryonic midbrain cells, but the role of oxidative damages is not clear in embryotoxicity.
에스트로겐 수용체를 통한 카드뮴 독성 및 항산화제에 의한 독성경감에 관한 연구
김태성(Tae Sung Kim),강태석(Tae Seok Kang),강호일(Hoil Kang),문현주(Hyun Ju Moon),강일현(Il Hyun Kang),이영주(Young Joo Lee),최은희(Eun Hee Choi),홍진태(Jin Tae Hong),한순영(Soon Young Han),홍진환(Jin Hwan Hong) 한국환경성돌연변이발암원학회 2006 한국환경성돌연변이·발암원학회지 Vol.26 No.1
Cadmium, a human carcinogen, can induce toxicity in various cell lines and organs. Despite extensive research, the mechanisms of cadmium-induced cell toxicity and estrogenic potential in human are not clear. This study was performed to investigate cadmium-induced toxicity on human breast cancer cells :MCF-7 cells, an estrogen receptor (ER) positive breast cancer cells, and MDA-MB-231 cells, an ER negative breast cancer cells. MCF-7 cells was proved to be more sensitive than the other cell lines (IC50 = 50 μM at MCF-7 cells and 120 μM at MDA-MB-231). The expression of JNK and AP-1 transcription factors such as c-Jun and c-Fos dependent transcription were increased by cadmium treatment. Inhibition of ER activation by ER antagonist (tamoxifen or ICI 182,780) significantly recovered the viablity and inhibited apoptotic cell death. This suggested that cadmium-induced cell death in ER (+) cells was mediated by JNK/AP-1 pathway and this pathway was more stimulated by ER activated by cadmium. Co-treatment of antioxidants such as selenium (Se), butylated hydroxyanisole (BHA), glutathione (GSH), or N-acetyl-L-cysteine (NAC) recovered the cadmium-induced cell death in MCF-7 cells. Cadmium-induced lipid peroxidation was decreased by GSH, NAC, or BHA in MCF-7 cells. The expression of SOD protein was decreased by cadmium (100 μM) but recovered by GSH, NAC, BHA, or Se. Our data showed that the cadmium-induced cell toxicity in human breast cancer cells could be protected by the antioxidants (Se, BHA, NAC, GSH, or NAC) and ER antagonist (tamoxifen or ICI 182,780). Therefore, toxicity of cadmium in breast cancer were mediated by oxidative stress and ERα.
1,2-Dimethylhydrazine에 의해 유발된 Colonic Aberrant Crypt Foci에 대한 마늘추출물의 암예방효과
김태명(Tae Myoung Kim),류재면(Jae Myun Ryu),권현정(Hyun Jung Kwon),황인국(In Guk Hwang),반정옥(Jung Ok Ban),정헌상(Heon Sang Jeong),홍진태(Jin Tae Hong),김대중(Dae Joong Kim) 한국독성학회 2007 Toxicological Research Vol.23 No.2
Garlic (Allium sativum L.) with the food supplement material and medicine was used traditionally in Asia and Europe. Epidemiological studies revealed that the intake of garlic reduced incidences of various cancer including digestive system. The present study was designed to investigate the effect of garlic ethanol extract on the development of colonic aberrant crypt foci (ACF) induced by 1,2-dimethylhydrazine (DMH) in male F344 rats. Five-week-old rats were given four times for two weeks to subcutaneous injections by DMH (30 ㎎/㎏ body weight) to induce ACF. The animals were divided into groups that fed diet containing garlic ethanol extract at five different doses (0.1, 0.2, 0.5, 2, 5%), respectively, animals were evaluated for the total number of ACF and total aberrant crypts (AC) per colon detected from methylene blue-stained rat colon. ACF were formed in animals in DMH-treated group. The feeding suppressed potently the appearance ACF in the colon of rats. Especially, fed diet containing garlic ethanol extract at intermediate dose (0.5%) significantly reduced the number of ACF and AC per colon (p < 0.05). Garlic ethanol extract inhibited DMH-induced overexpression of Activator Protein-1 (AP-1) and β-catenin genes related to cell proliferation that also upregulated the expression of p21Waf1/Cip1 mRNA, a cell cycle-regulating gene. These results suggested that garlic ethanol extract may inhibit ACF formation, β-catenin gene as the early preneoplastic marker of malignant potential in the process of colon carcinogenesis.