Department of Ophthalmology, Taipei Medical University Hospital, Taipei Taiwan.
J Biomed Sci. 2011 Feb 5;18(1):11. doi: 10.1186/1423-0127-18-11.
Taurine has chemical structure similar to an inhibitory neurotransmitter, γ-aminobutyric acid (GABA). Previous studies on GABA in the stomach suggest GABAergic neuron is involved in acid secretion, but the effects of taurine are poor understood.
The effects of taurine on acid secretion, signal transduction, and localization of taurinergic neurons were determined in the rat stomach using everted whole stomach, RIA kit and immunohistochemical methods.
We used antibodies against taurine-synthesizing enzyme, cysteine sulfuric acid decarboxylase (CSAD), and taurine. CSAD- and taurine-positive cells were found in the muscle and mucosal layers. Distributions of CSAD- and taurine-positive cells in both mucosal and muscle layers were heterogeneous in the stomach. Taurine at 10-9~10-4 M induced acid secretion, and the maximum secretion was at 10-5 M, 1.6-fold higher than the spontaneous secretion. Taurine-induced acid secretion was completely inhibited by bicuculline and atropine but not by cimetidine, proglumide, or strychnine. Atropine and tetrodotoxin (TTX) completely inhibited the acid secretion induced by low concentrations of taurine and partially inhibited induced by high concentrations. Verapamil, a calcium blocker agent, inhibited acid output elicited by taurine. We assumed all Ca2+ channels involved in the response to these secretagogues were equally affected by verapamil. Intracellular cAMP (adenosine 3', 5'-monophosphate) in the stomach significantly increased with taurine treatment in a dose-dependent manner. High correlation (r=0.859, p < 0.001) of taurine concentrations with cAMP was observed.
Our results demonstrated for the first time in taurine-induced acid secretion due to increase intracellular calcium may act through the A type of GABA receptors, which are mainly located on cholinergic neurons though cAMP pathway and partially on nonneuronal cells in the rat stomach.
牛磺酸的化学结构与抑制性神经递质γ-氨基丁酸(GABA)相似。先前关于胃中 GABA 的研究表明,GABA 能神经元参与胃酸分泌,但牛磺酸的作用尚不清楚。
采用外翻胃法、放射免疫试剂盒和免疫组织化学方法,在大鼠胃中研究牛磺酸对胃酸分泌、信号转导和牛磺酸能神经元定位的影响。
我们使用针对牛磺酸合成酶半胱氨酸硫酸脱羧酶(CSAD)和牛磺酸的抗体。CSAD 和牛磺酸阳性细胞存在于肌肉和黏膜层中。胃黏膜和肌肉层中 CSAD 和牛磺酸阳性细胞的分布不均匀。10-9~10-4 M 的牛磺酸诱导胃酸分泌,最大分泌量在 10-5 M 时达到 1.6 倍,高于自发分泌量。牛磺酸诱导的胃酸分泌完全被荷包牡丹碱和阿托品抑制,但不受西咪替丁、丙谷胺或士的宁抑制。阿托品和河豚毒素(TTX)完全抑制低浓度牛磺酸诱导的胃酸分泌,部分抑制高浓度牛磺酸诱导的胃酸分泌。钙通道阻滞剂维拉帕米抑制牛磺酸引起的胃酸分泌。我们假设这些激动剂引起的反应中涉及的所有 Ca2+ 通道都受到维拉帕米的同等影响。胃内细胞内环磷酸腺苷(cAMP)随着牛磺酸处理呈剂量依赖性显著增加。观察到牛磺酸浓度与 cAMP 之间存在高度相关性(r=0.859,p<0.001)。
我们的研究结果首次证明,牛磺酸诱导的胃酸分泌增加可能是由于细胞内钙增加,通过 A 型 GABA 受体发挥作用,这些受体主要位于大鼠胃中的胆碱能神经元上,但部分位于非神经元细胞上,通过 cAMP 途径发挥作用。