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題 名 | Pharmacologic Agents Inhibit Rat Mesangial Cell Proliferation and Collagen Synthesis=抑制老鼠腎絲球間質細胞生長及膠原蛋白合成之藥物 |
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作 者 | 方震中; 嚴崇仁; 徐仁熙; 吳明修; 蔡敦仁; 謝博生; | 書刊名 | 臺灣醫學會雜誌 |
卷 期 | 97:7 1998.07[民87.07] |
頁 次 | 頁458-464 |
分類號 | 418.41 |
關鍵詞 | 抑制; 老鼠; 腎絲球間質細胞生長; 膠原蛋白; 藥品合成; Aminophyline; cAMP; Collagen synthesis; Hydralazine; Mesangial cell; Nicametate; Ticlopidine; |
語 文 | 英文(English) |
英文摘要 | Prevention of the development of end-stage renal disease is one of the most promising areas of research in nephrology. Because mesangial cell proliferation and extracellular matrix accumulation have been regarded as antecedents of glomerulosclerosis, agents that can inhibit mesangial cell proliferation may have a potential to retard the progression of renal diseases. Therefore, we investigated several clinically available agents that might affect mesangial cell proliferation and collagen synthesis in male Sprague-Dawley rats. Cell proliferation was measured by the tetrazolium dye uptake method. Collagen synthesis was measured by �鯨-proline incorporation into pepsin-resistant, salt-precipitated collagen. Intracellular cAMP levels were measured by enzyme immunoassay. Our results showed that hydralazine (82% inhibition at 10 μ g/mL), ticlopidine (61% inhibition at 30 μ g/mL), aminophylline (66% inhibition at 200 μ g/mL ), and nicametate (91% inhibition at 1 μ g/mL) inhibited serum -stimulated rat mesangial cell (RMC) growth in a dosedependent manner. Ticlopidine (43% inhibition at 30 μ g/mL), aminophylline (52% inhibition at 200 μ g/mL), and nicametate (35% inhibition at 1 μ g/mL) inhibited collagen synthesis in confluent RMCs. Aminophylline may act through increasing intracellular cAMP levels (9.7 ± 0.7 pmol/mg protein at 200 μ g /mL of aminophyllin vs 4.2 ± 0.6 pmol/mg protein at control). These data suggest that aminophylline, ticlopidine, hydralazine, and nicametate can inhibit RMC proliferation and collagen synthesis. |
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