頁籤選單縮合
題 名 | Effect of NPC-15199 on Ca[fec7] Levels in Renal Tubular Cells |
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作 者 | Jan,Chung-ren; Jiann,Bang-ping; Chang,Hong-tai; Yu,Cha-chen; Lu,Yih-chau; Yeh,Jeng-hsien; Chen,Wei-chun; Law,Yee-ping; Huang,Jong-khing; | 書刊名 | 中國生理學雜誌 |
卷 期 | 45:3 2002.09[民91.09] |
頁 次 | 頁117-122 |
分類號 | 394.72 |
關鍵詞 | Ca[fec7]; Ca[fec7]stores; Fura-2; MDCK; NPC-15199; Renal tubular cells; |
語 文 | 英文(English) |
英文摘要 | In Madin-Darby canine kidney (MDCK) cells, effect of NPC-15199 on intracellular □ concentration □ was investigated by using fura-2. NPC 15199 (100-1000 μM) caused a rapid and sustained increase of □ in a concentration-dependent manner (E□=500 μM). NPC-15199-induced □ rise was prevented by 70$ by removal of extracellular □, but was not changed by dihydro-pyridines, verapamil and diltiazem. In □ –free medium, carbonylcyanide m-chlorophyenylhydrazone (CCCP; 2 μM), a mitochondrial uncoupler, and thapsigargin (1 μM), and inhibitor of the endoplasmic reticulum (ER) □ –ATPase, caused a monophasic □ rise, respectively, after which the increasing effect of NPC-15199 (1mM) on □ was substantially attenuated; also, pretreatment with NPC-15199 abolished CCCP- and thapsigargin-induced □ rises. U73122, an inhibitor of phosipholipase C, abolished 10 μM ATP (but not 1 mM NPC-15199)-induced □ rise. These results suggest that NPC-15199 rapidly increases □ by stimulating both extracellular □ influx and intracellular □ release via as yet unidentified mechanisms(s). |
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