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作 者:周洁琼[1] 黄峥嵘[1] 李卫华[1] 谢强[1]
出 处:《中华老年医学杂志》2014年第5期539-542,共4页Chinese Journal of Geriatrics
基 金:国家自然科学基金(81170090)
摘 要:目的 观察辛伐他汀对小鼠胰岛β细胞株MIN6 三磷酸腺苷敏感性钾通道(KATP)和L型钙通道(L-Ca)电流的影响. 方法 将MIN6细胞分0.05%二甲基亚砜(DMSO)组、正常对照组和低、中、高浓度辛伐他汀组,分别用含0.05% DMSO和含0、2、5、10 μmol/L辛伐他汀浓度的15%胎牛血清高糖DMEM培养基培养48 h.采用全细胞膜片钳技术记录细胞KATP和L-Ca电流. 结果 MIN6细胞正常细胞外液灌流时KATP最大电流密度为(92.81±4.10) pA/pF,用含2、5及10μmol/L浓度辛伐他汀培养基培养48 h后细胞钾电流增加,分别为(117.94±3.67) pA/pF、(153.91±12.38) pA/pF、(307.01±6.40) pA/pF(均P<0.01).MIN6细胞高糖细胞外液灌流时LCa最大电流密度为(-21.03±0.55)pA/pF,3种浓度辛伐他汀培养基干预后的电流密度分别降至(-16.31±0.51) pA/pF、(-10.75±0.71)pA/pF、(3.30±0.46) pA/pF(均P<0.01). 结论 辛伐他汀对小鼠胰岛β细胞株MIN6细胞KATP电流具有增大作用,对L-Ca电流有减小作用,从而影响胰岛素的分泌,从而影响糖代谢.Objective To observe the influence of Simvastatin on the ATP-sensitive K+Channels and L-type Ca2+ Channels in mouse pancreatic beta cell line MIN6.Methods MIN6 cells were divided into 0.05 % dimethyl sulfoxide (DMSO) group,normal control group and low-,middle-,high-concentration of Simvastatin treatment groups,that were cultured for 48 h with high-glucose DMEM containing 15% fetal bovine serum plus 0.05% dimethyl sulfoxide,0,2,5 and 10 μmol/Lsimvastatin,respectively.Whole-cell patch-clamp technology was used to record the currents of ATP-sensitive K+ channels and L-type Ca2+ channels in MIN6 cells.Results The mean potassium current density in normal external solution perfusion group was (92.81 ±4.10) pA/pF.Compared with normal external solution perfusion control group,2,5 and 10 μmol/L Simvastatin treatments markedly enhanced the current density of ATP-sensitive K+ Channels,reaching to (117.94 ± 3.67)pA/pF,(153.91±12.38) pA/pF,(307.01±6.40) pA/pF (all P〈0.01),respectively.The current density in L-type Ca2+ Channels was (-21.03 ± 0.55) pA/pF in glucose external solution group.Compared with glucose external solution group,the current density in 2,5 and 10 μmol/L Simvastatin treatment groups were decreased to (16.31±0.51) pA/pF,(-10.75±0.71) pA/pF,(-3.30±0.46) pA/pF (all P〈0.01),respectively.Conclusions Simvastatin inhibits insulin secretion and glycometabolism in mouse pancreatic beta cell line MIN6 via enhancing the current density of ATP-sensitive K+ Channels and inhibiting the current density of L-type Ca2+ Channels.
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