摘要
目的 探讨川芎嗪刺激结肠黏膜分泌阴离子的信号转导机制。方法 运用某些工具药 ,采用短路电流技术观察了川芎嗪促进大鼠远端结肠黏膜分泌阴离子的信号转导机制。结果 结肠黏膜的基底膜加入 1mmoL/L的川芎嗪后 ,短路电流明显增加 ,在 3 0分钟内转运的电荷数增加了 3 7.5± 5 .1mC/cm2 (n =12 ) ;黏膜的基底膜和腔面膜预先加入PKA的抑制剂 -H89(0 .0 48μmoL/L)后 ,川芎嗪所产生的电荷数为 9.1± 2 .5mC/cm2 (n =8) ,相对于对照组 ,减少大约 76% (P <0 .0 0 1) ;在黏膜的基底膜预先加入前列腺素环化酶抑制剂 -吲哚美辛 (10 μmoL/L)后 ,川芎嗪所产生的电荷数为 11.4± 4.0mC/cm2 (n =9) ,相对于对照组 ,减少大约 70 % (P <0 .0 0 1) ;在黏膜的基底膜预先加入Ca2 +螯合剂 -BAPTA -AM(10 0 μmoL/L)后 ,川芎嗪所产生的电荷数为 2 0 .5± 7.3mC/cm2 (n =5 ) ,相对于对照组 ,减少大约 45 % (P <0 .0 5 )。结论 川芎嗪可以通过细胞内的前列腺素 /cAMP和Ca2
Objective To investigate the underlying cellular signaling transduction mechanism in the effect of ligustrazine on the secretion of colonic mucosa. Methods Using short circuit current (Isc) technique in conjunction with “Tool drugs', the signaling transduction mechanism in the effect of ligustrazine on the secretion of colonic mucosa was investigated.Results Basolateral application of 1mmol/L TMP produced an increase in Isc and the total charges transported for 30 minutes was about 37.5 +5.1mC/cm 2;bilateral pretreatment of H 89 (0. 048μmoL/L), the inhibitor of PKA, decreased the TMP-induced Isc by about 76%( P <0.001 ).The basolateral presence of indomethacin (10μmoL/L), a prostaglandin synthesis inhibitor significantly reduced the TMP evoked Isc by about 70% ( P <0.001);basolateral addition of Ca 2+ chelator, BAPTA AM(100μmoL/L), reduced the TMP evoked Isc by about 45% ( P <0.05).Conclusion Ligustrazine could promote colonic mucosa secrete anion via intracellular prostaglandin/cAMP and Ca 2+ .
出处
《胃肠病学和肝病学杂志》
CAS
2004年第4期388-390,共3页
Chinese Journal of Gastroenterology and Hepatology
