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박봉주,박종철,Hideaki Taguchi,Katsuhiko Kamei,Tetsuhiro Matsuzawa,현성휴 연세대학교의과대학 2011 Yonsei medical journal Vol.52 No.3
Previously, we reported that epigallocatechin 3-O-gallate (EGCg) has growth-inhibitory effect on clinical isolates of Candida species. In this study, we investigated the antifungal activity of EGCg and antifungal agents against thirty-five of dermatophytes clinically isolated by the international guidelines (M38-A2). All isolates exhibited good susceptibility to EGCg (MIC_50, 2-4 μg/mL, MIC_90, 4-8 μg/mL, and geometric mean (GM) MICs, 3.36-4 μg/mL) than those of fluconazole (MIC_50, 2-16 μg/mL, MIC_90, 4-32 μg/mL, and GM MICs, 3.45-25.8 μg/mL) and flucytosin (MIC_50, MIC_90, and GM MICs, >64 μg/mL), although they were less susceptible to other antifungal agents, such as amphotericin B, itraconazole, and miconazole. These activities of EGCg were approximately 4-fold higher than those of fluconazole, and were 4 to 16-fold higher than flucytosin. This result indicates that EGCg can inhibit pathogenic dermatophyte species. Therefore, we suggest that EGCg may be effectively used solely as a possible agent or combined with other antifungal agents for antifungal therapy in dermatophytosis.
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한동욱,박종철,임혜련,조한희,Kazuaki Matsumura,백현숙,이미희,우연이,현성휴 한국생체재료학회 2006 생체재료학회지 Vol.10 No.1
The migration of vascular smooth muscle cells (VSMCs) from the tunica media to the subendothelial region is a key event in the development and progression of atherosclerosis and post-angioplasty vascular remodeling. The abnormal growth of VSMC also plays an important role in vascular diseases, including arteriosclerosis and restenosis after angioplasty. Many in vitro assays have shown that ()-epigallocatechin-3-O-gallate (EGCG) has antiproliferative effects on various cells. In this study, the proliferation of rat aortic SMCs (RASMCs) with serum stimulation were investigated into EGCG-loaded collagen matrices (EGCG-CM). Also, the effect of EGCG-CM was examined on the migration of serum-stimulated RASMCs. RASMCs were primarily cultured from rat aorta and then characterized by using immunocytochemical analysis with -smooth muscle actin antibody. EGCG treatment to RASMCs showed a dose-dependent decrease in cell viability as increase in its concentration. EGCG-CM was fabricated by freeze-drying at -40oC and then loaded with EGCG. The proliferation of RASMCs cultured into EGCG-CM was significantly (p < 0.05) attenuated in spite of serum induction (reduction by about 30% after 3 d of cultures and 39% after 5 d). While RASMCs migrated toward CM in response to serum and populated it with essentially uniform ingrowth, EGCG-CM considerably blocked the cell migration after 3 d of incubation. These results suggest that reduction in the proliferation and migration of RASMCs induced by serum may be mediated through the inhibitory effects of EGCG released from CM
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