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The Underlying Cellular mechanism in the Effect of Ligustrazine on the Anion Secretion of Colonic Mucosa

机译:川gust嗪对结肠粘膜阴离子分泌影响的潜在细胞机制

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Aim: To investigate the underlying cellular mechanism in the effect of ligustrazine on anion secretion of colonic mucosa. Methods: Sheets of rat distal colon were mounted in Ussing chambers and the electrolyte transport was analyzed using short-circuit current (I_(SC)) technique in conjunction with "Tool drugs". Results: (1) In HCO3~--free K-H solution, basolateral application of Immol/L TMP produced an increase in Isc and the total charges transported in 30 minutes was about 8.3 ± 1.9mC/cm~2; Apical pretreatment of DPC(1mmoL/L), the inhibitor of Cl~- channels, decreased the TMP-induced Isc by about 84% (P < 0.01) ; The basolateral presence of bumetanide (0.1mmoL/L), the inhibitor of Na~+-K~+-Cl~- cotransporter (NKCC), significantly reduced the TMP-evoked Isc by about 86% (P < 0.01). (2) In Cl~--free K-H solution, basolateral application of Immol/L TMP produced an increase in Isc and the total charges transported for 30 minutes was about 8.7 ± 1.4mC/cm~2; Apical pretreatment of DPC and basolateral addition of acetazolamide decreased the TMP-induced Isc by about 60% (P < 0.01) and 45%(P < 0.05) respectively; Basolateral application of DIDS, the inhibitor of Na~+-HCO_3~- cotransporter (NBC), didn't alter the TMP-induced Isc. Conclusion: (1) Ligustrazine could promote colonic mucosa secrete Cl~- via apical Cl~- channels and basolateral NKCC. (2) Ligustrazine could promote colonic mucosa secrete HCO_3~- via apical Cl~- channels and basolateral diffusion of CO_2.
机译:目的:探讨川gust嗪对结肠黏膜阴离子分泌的影响的潜在细胞机制。方法:将大鼠远端结肠片装在Ussing室中,并结合“工具药物”使用短路电流(I_(SC))技术分析电解质的运输。结果:(1)在无HCO3〜-的K-H溶液中,Immol / L TMP的基底外侧施用增加了Isc,并且在30分钟内传输的总电荷约为8.3±1.9mC / cm〜2; Cl〜-通道抑制剂DPC(1mmoL / L)的根尖预处理可使TMP诱导的Isc降低约84%(P <0.01); Na + -K-+-Cl--共转运蛋白(NKCC)抑制剂布美他尼的基底外侧(0.1mmoL / L)显着降低了TMP诱发的Isc约86%(P <0.01)。 (2)在无氯的K-H溶液中,基底侧施用Immol / L TMP产生了Isc的增加,并且输送30分钟的总电荷约为8.7±1.4mC / cm〜2。 DPC的根尖预处理和乙酰唑胺的基底外侧添加分别使TMP诱导的Isc降低约60%(P <0.01)和45%(P <0.05)。 Na〜+ -HCO_3〜-共转运蛋白(NBC)的抑制剂DIDS在基底外侧的应用并没有改变TMP诱导的Isc。结论:(1)川gust嗪可通过顶叶Cl〜-通道和基底外侧NKCC促进结肠黏膜分泌Cl〜-。 (2)川gust嗪可通过顶叶Cl〜-通道和CO_2的基底外侧扩散促进结肠黏膜分泌HCO_3〜-。

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