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Phellinus linteus, Phellinus baumii 및 Phellinus gilvus 자실체 추출물의 항암효과 비교
배재성(Jae-Sung Bae),황미현(Mi-Hyun Hwang),장광호(Kwang-Ho Jang),이만휘(Man-Hee Rhee),이근우(Keun-Woo Lee),조우식(Woo-Sik Jo),최성국(Sung-Kuk Choi),윤효인(Hyo-In Yun),임종환(Jong-Hwan Lim),김종춘(Jong-Choon Kim),박승춘(Seung-Chun Par 한국독성학회 2004 Toxicological Research Vol.20 No.1
This study was undertaken to investigate comparative anti-tumor activity of water extracts of Phellinus gilvus (PGE), Phellinus linteus (PLE), and Phellinus baumii (PBE) in vitro. The anti-tumor activity in the present study was evaluated by sulforhodamine B (SRB) and microtetrazolium (MTT) assay in terms of cell survival level. The tumor cells (sarcoma 180 and P388) were treated with PGE, PLE, and PBE (7.5, 15, and 30 mg/ml) and Doxorubicin (DOX) (0.001~10 mM). The results showed that DOX, PGE, and PLE inhibited proliferation showing a dose-dependent manner against both tumor cells. However, PBE was inhibited by the only 30 mg/ml in both cells proliferation. In conclusion, all of PGE, PLE, and PBE used in this study have shown anti-tumor activity against both sarcoma 180 and P388. Among them, PLE was the most effective in anti-tumor activity against sarcoma 180 (p<0.05) and PGE was against P388 in SRB assay. PLE, however, was against P388 (p<0.05) in MTT assay.
( Ae Rin Baek ),( Ji Min Lee ),( Hyun Jung Seo ),( Jong Sook Park ),( June Hyuk Lee ),( Sung Woo Park ),( An Soo Jang ),( Do Jin Kim ),( Eun Suk Koh ),( Soo Taek Uh ),( Yong Hoon Kim ),( Choon Sik Par 대한결핵 및 호흡기학회 2016 Tuberculosis and Respiratory Diseases Vol.79 No.3
Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by the accumulation of excessive fibroblasts and myofibroblasts in the extracellular matrix. The transforming growth factor β1 (TGF-β1).induced epithelial-to-mesenchymal transition (EMT) is thought to be a possible source of fibroblasts/ myofibroblasts in IPF lungs. We have previously reported that apolipoprotein A1 (ApoA1) has anti-fibrotic activity in experimental lung fibrosis. In this study, we determine whether ApoA1 modulates TGF-β1.induced EMT in experimental lung fibrosis and clarify its mechanism of action. Methods: The A549 alveolar epithelial cell line was treated with TGF-β1 with or without ApoA1. Morphological changes and expression of EMT-related markers, including E-cadherin, N-cadherin, and α-smooth muscle actin were evaluated. Expressions of Smad and non-Smad mediators and TGF-β1 receptor type 1 (TβRI) and type 2 (TβRII) were measured. The silica-induced lung fibrosis model was established using ApoA1 overexpressing transgenic mice. Results: TGF-β1.treated A549 cells were changed to the mesenchymal morphology with less E-cadherin and more N-cadherin expression. The addition of ApoA1 inhibited the TGF-β1.induced change of the EMT phenotype. ApoA1 inhibited the TGF-β1.induced increase in the phosphorylation of Smad2 and 3 as well as that of ERK and p38 mitogenactivated protein kinase mediators. In addition, ApoA1 reduced the TGF-β1.induced increase in TβRI and TβRII expression. In a mouse model of silica-induced lung fibrosis, ApoA1 overexpression reduced the silica-mediated effects, which were increased N-cadherin and decreased E-cadherin expression in the alveolar epithelium. Conclusion: Our data demonstrate that ApoA1 inhibits TGF-β1.induced EMT in experimental lung fibrosis.