AIM: To investigate the effect of gingerol on colonic motility and the action of L-type calcium channel currents in this process.METHODS: The distal colon was cut along the mesenteric border and cleaned with Ca^(2+)-f...AIM: To investigate the effect of gingerol on colonic motility and the action of L-type calcium channel currents in this process.METHODS: The distal colon was cut along the mesenteric border and cleaned with Ca^(2+)-free physiological saline solution. Muscle strips were removed and placed in Ca^(2+)-free physiological saline solution, which was oxygenated continuously. Longitudinal smooth muscle samples were prepared by cutting along the muscle strips and were then placed in a chamber. Mechanical contractile activities of isolated colonic segments in rats were recorded by a 4-channel physiograph. Colon smooth muscle cells were dissociated by enzymatic digestion. L-type calcium currents were recorded using the conventional whole-cell patch-clamp technique.RESULTS: Gingerol inhibited the spontaneous contraction of colonic longitudinal smooth muscle in a dose-dependent manner with inhibition percentages of 13.3% ± 4.1%, 43.4% ± 3.9%, 78.2% ± 3.6% and 80.5% ± 4.5% at 25 μmol/L, 50 μmol/L, 75 μmol/L and 100 μmol/L, respectively(P < 0.01). Nifedipine, an L-type calcium channel blocker, diminished the inhibition of colonic motility by gingerol. Gingerol inhibited L-type calcium channel currents in colonic longitudinal myocytes of rats. At a 75 μmol/L concentration of gingerol, the percentage of gingerolinduced inhibition was diminished by nifedipine from 77.1% ± 4.2% to 42.6% ± 3.6%(P < 0.01). Gingerol suppressed IBa in a dose-dependent manner, and the inhibition rates were 22.7% ± 2.38%, 35.77% ± 3.14%, 49.78% ± 3.48% and 53.78% ± 4.16% of control at 0 m V, respectively, at concentrations of 25 μmol/L, 50 μmol/L, 75 μmol/L and 100 μmol/L(P < 0.01). The steady-state activation curve was shifted to the right by treatment with gingerol. The value of half activation was-14.23 ± 1.12 m V in the control group and-10.56 ± 1.04 m V in the 75 μmol/L group(P < 0.05) with slope factors, Ks, of 7.16 ± 0.84 and 7.02 ± 0.93(P < 0.05) in the control and 75 μmol/L groups, respectively. However, the steady-state inactivation curve was not changed, with a half-inactivation voltage, 0.5 V, of-27.43 ± 1.26 m V in the control group and-26.56 ± 1.53 m V in the 75 μmol/L gingerol group(P > 0.05), and a slope factor, K, of 13.24 ± 1.62 in the control group and 13.45 ± 1.68(P > 0.05) in the 75 μmol/L gingerol group.CONCLUSION: Gingerol inhibits colonic motility by preventing Ca^(2+) influx through L-type calcium channels.展开更多
目的:探讨参松养心胶囊对大鼠心室肌细胞L-型钙电流(Ica,L)和瞬时外向钾电流(Ito)的抑制作用。方法:酶解法分离大鼠心室肌细胞,使用参松养心溶液(0.5 mg/100 m L,0.5%)灌流心室肌细胞,利用全细胞膜片钳技术记录Ica,L和Ito,在细胞破膜后...目的:探讨参松养心胶囊对大鼠心室肌细胞L-型钙电流(Ica,L)和瞬时外向钾电流(Ito)的抑制作用。方法:酶解法分离大鼠心室肌细胞,使用参松养心溶液(0.5 mg/100 m L,0.5%)灌流心室肌细胞,利用全细胞膜片钳技术记录Ica,L和Ito,在细胞破膜后的20 min内记录所有数据,对每个细胞给药前后做自身对照,观察参松养心溶液对Ica,L和Ito通道电流的影响。结果:0.5%的参松养心溶液对Ica,L和Ito均有抑制作用,参松养心溶液对Ito的缓慢电流成分Itos无明显作用,但可以明显抑制Ito的快速电流成分Itof。在-10 m V测试电压下,在0.5%的参松养心溶液作用后,Ica,L的最大激活峰值电流密度从(-8.64+-2.43)p A/p F降为(-5.92+-2.15)p A/p F,抑制率为31.85%+10.25%,电流密度-电压(I-V)曲线上移;在-60 m V测试电压下,在0.5%的参松养心溶液作用后,Itof的最大激活峰值电流密度从(23.53+3.31)p A/p F降为(16.86+2.34)p A/p F,抑制率为(28.33+10.59)%,I-V曲线下移。参松养心溶液不改变Ica,L的通道动力学,但会使Ito通道失活后的恢复变慢。结论:参松养心溶液对Ica,L和Ito均有明显的抑制作用。展开更多
基金Supported by National Basic Research Program of China(973 Program)No.2013CB531703+3 种基金National Natural Science Foundation of ChinaNo.81273919Natural Science Foundation of Liaoning ProvinceNo.2012225020 and No.2013023002
文摘AIM: To investigate the effect of gingerol on colonic motility and the action of L-type calcium channel currents in this process.METHODS: The distal colon was cut along the mesenteric border and cleaned with Ca^(2+)-free physiological saline solution. Muscle strips were removed and placed in Ca^(2+)-free physiological saline solution, which was oxygenated continuously. Longitudinal smooth muscle samples were prepared by cutting along the muscle strips and were then placed in a chamber. Mechanical contractile activities of isolated colonic segments in rats were recorded by a 4-channel physiograph. Colon smooth muscle cells were dissociated by enzymatic digestion. L-type calcium currents were recorded using the conventional whole-cell patch-clamp technique.RESULTS: Gingerol inhibited the spontaneous contraction of colonic longitudinal smooth muscle in a dose-dependent manner with inhibition percentages of 13.3% ± 4.1%, 43.4% ± 3.9%, 78.2% ± 3.6% and 80.5% ± 4.5% at 25 μmol/L, 50 μmol/L, 75 μmol/L and 100 μmol/L, respectively(P < 0.01). Nifedipine, an L-type calcium channel blocker, diminished the inhibition of colonic motility by gingerol. Gingerol inhibited L-type calcium channel currents in colonic longitudinal myocytes of rats. At a 75 μmol/L concentration of gingerol, the percentage of gingerolinduced inhibition was diminished by nifedipine from 77.1% ± 4.2% to 42.6% ± 3.6%(P < 0.01). Gingerol suppressed IBa in a dose-dependent manner, and the inhibition rates were 22.7% ± 2.38%, 35.77% ± 3.14%, 49.78% ± 3.48% and 53.78% ± 4.16% of control at 0 m V, respectively, at concentrations of 25 μmol/L, 50 μmol/L, 75 μmol/L and 100 μmol/L(P < 0.01). The steady-state activation curve was shifted to the right by treatment with gingerol. The value of half activation was-14.23 ± 1.12 m V in the control group and-10.56 ± 1.04 m V in the 75 μmol/L group(P < 0.05) with slope factors, Ks, of 7.16 ± 0.84 and 7.02 ± 0.93(P < 0.05) in the control and 75 μmol/L groups, respectively. However, the steady-state inactivation curve was not changed, with a half-inactivation voltage, 0.5 V, of-27.43 ± 1.26 m V in the control group and-26.56 ± 1.53 m V in the 75 μmol/L gingerol group(P > 0.05), and a slope factor, K, of 13.24 ± 1.62 in the control group and 13.45 ± 1.68(P > 0.05) in the 75 μmol/L gingerol group.CONCLUSION: Gingerol inhibits colonic motility by preventing Ca^(2+) influx through L-type calcium channels.
