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Effects of Ca^2+ channel blockers on store-operated Ca^2+ channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats
引用本文:Jiang N,Zhang ZM,Liu L,Zhang C,Zhang YL,Zhang ZC. Effects of Ca^2+ channel blockers on store-operated Ca^2+ channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats[J]. World journal of gastroenterology : WJG, 2006, 12(29): 4694-4698. DOI: 10.3748/wjg.v12.i29.4694
作者姓名:Jiang N  Zhang ZM  Liu L  Zhang C  Zhang YL  Zhang ZC
基金项目:国家高技术研究发展计划(863计划);教育部资助项目;上海市教委"曙光计划"
摘    要:


关 键 词:钙离子通道  肝损伤  缺血再灌注损伤  病理机制
收稿时间:2006-01-12

Effects of Ca2+ channel blockers on store-operated Ca2+ channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats
Jiang Nan,Zhang Zong-Ming,Liu Liang,Zhang Chi,Zhang Yan-Lu,Zhang Zi-Chao. Effects of Ca2+ channel blockers on store-operated Ca2+ channel currents of Kupffer cells after hepatic ischemia/reperfusion injury in rats[J]. World journal of gastroenterology : WJG, 2006, 12(29): 4694-4698. DOI: 10.3748/wjg.v12.i29.4694
Authors:Jiang Nan  Zhang Zong-Ming  Liu Liang  Zhang Chi  Zhang Yan-Lu  Zhang Zi-Chao
Affiliation:1. Department of General Surgery,Digestive Medical Center, First Affiliated Hospital of Tsinghua University, Beijing 100016, China
2. Department of 1st General Surgery of Tongji Hospital, Tongji University, Shanghai 200065, China
Abstract:
AIM: To study the effects of hepatic ischemia/reperfusion (I/R) injury on store-operated calcium channel (SOC) currents (I(SOC)) in freshly isolated rat Kupffer cells, and the effects of Ca(2+) channel blockers, 2-aminoethoxydiphenyl borate (2-APB), SK and F96365, econazole and miconazole, on I(SOC) in isolated rat Kupffer cells after hepatic I/R injury. METHODS: The model of rat hepatic I/R injury was established. Whole-cell patch-clamp techniques were performed to investigate the effects of 2-APB, SK and F96365, econazole and miconazole on I(SOC) in isolated rat Kupffer cells after hepatic I /R injury. RESULTS: I/R injury significantly increased I(SOC) from -80.4 +/- 25.2pA to -159.5 +/- 34.5pA ((b)P < 0.01, n = 30). 2-APB (20, 40, 60, 80, 100 micromol/L), SK and F96365 (5, 10, 20, 40, 50 micromol/L), econazole (0.1, 0.3, 1, 3, 10 micromol/L) and miconazole (0.1, 0.3, 1, 3, 10 micromol/L) inhibited I(SOC) in a concentration-dependent manner with IC50 of 37.41 micromol/L (n = 8), 5.89 micromol/L (n = 11), 0.21 micromol/L (n = 13), and 0.28 micromol/L (n = 10). The peak value of I(SOC) in the I-V relationship was decreased by the blockers in different concentrations, but the reverse potential of I(SOC) was not transformed. CONCLUSION: SOC is the main channel for the influx of Ca(2+) during hepatic I/R injuries. Calcium channel blockers, 2-APB, SK and F96365, econazole and miconazole, have obviously protective effects on I/R injury, probably by inhibiting I(SOC) in Kupffer cells and preventing the activation of Kupffer cells.
Keywords:Kupffer cell  Ischemia/reperfusion  Storeoperated calcium channel currents  2-aminoethoxydiphenyl borate  SK&F96365  Econazole  Miconazole
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