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本研究用短路电流技术来观察在川芎嗪作用下,电解质在大鼠远端结肠上皮细胞的转运及其细胞机制。在新鲜分离的结肠上皮的基侧膜加入川芎嗪,能产生较大的短路电流。用粘膜下神经元阻断剂——河豚毒素预作用于结肠上皮,不影响随后的川芎嗪所产生的短路电流,前列腺素合成抑制剂indomethacin预作用可使随后的川芎嗪产生的短路电流减少55.2％。在结肠上皮的顶膜加入C1-通道阻断剂。DPC和glibenclamide,能完全阻断川芎嗪产生的短路电流。Bumetanide,基侧膜钠、钾、氯共转运体阻断剂能抑制川芎嗪引起的短路电流的85.2％,而结肠上皮细胞基侧膜的非选择性钾通道阻断剂Ba2+能阻断90％以上的短路电流,说明基侧膜的钠、钾、氯共转运体和钾通道在川芎嗪引起的短路电流中起着重要的作用。上述结果表明,川芎嗪刺激大鼠远端结肠上皮细胞分泌C1-是通过上皮细胞顶膜C1-通道和基侧膜的钠、钾、氯共转体和K+通道介导的。
This study used short-circuit current technology to observe the transport of electrolytes in rat distal epithelial cells under the action of tetramethylpyrazine and its cellular mechanism. The addition of tetramethylpyrazine to the basement membrane of freshly isolated colonic epithelium can generate large short-circuit currents. The use of submucosal neuron blocker, tetrodotoxin, pre-acts on the colonic epithelium without affecting the short-circuit current generated by the subsequent ligustrazine. The prostaglandin synthesis inhibitor indomethacin pre-action can reduce the short-circuit current generated by the following tetramethylpyrazine by 55.2. %. A C1-channel blocker was added to the apical membrane of the colonic epithelium. DPC and glibenclamide can completely block the short-circuit current generated by ligustrazine. Bumetanide, a basal membrane sodium, potassium, and chlorine co-transporter blocker inhibited 85.2% of the short-circuit current caused by tetramethylpyrazine, while Ba2+, a non-selective potassium channel blocker of the basolateral membrane of colonic epithelial cells, blocked 90%. The above short-circuit currents indicate that the sodium, potassium, chlorine co-transporters and potassium channels of the basal membrane play an important role in the short-circuit currents induced by tetramethylpyrazine. The above results indicate that Ligustrazine stimulates secretion of C1- from distal colonic epithelial cells of rats, which is mediated by the sodium, potassium, and chlorine co-rotators and K+ channels of the epithelial cell apical membrane C1-channel and basolateral membrane.