Amos S, Binda L, Kunle O F, Okafor I, Emeje M, Akah P A, Wambebe C, Gamaniel K
Department of Pharmacology and Toxicology, National Institute for Pharmaceutical Research and Development, Abuja, Nigeria.
Phytother Res. 2003 Aug;17(7):792-6. doi: 10.1002/ptr.1239.
The contractile effects of the aqueous extract of the leaves of Indigofera dendroides (ID) were studied on the gastrointestinal motility in mice and isolated smooth muscle preparations obtained from rats and guinea pigs. The contractile effects of 10(-6) M acetylcholine, 80 mM KCl and 1.6 mg/ml ID were measured on the rat ileal smooth muscle exposed to calcium-free buffer or physiological solution, to determine the calcium pools mobilized by extract for activation of contraction. Acute toxicity test (LD(50)) was also carried out in mice. The result showed that ID (0.05-3.2 mg/ml) produced a concentration-dependent contraction of the guinea pig and rat ileum. These responses were not blocked by mepyramine (2.49 x 10(-9) M), verapamil (8.14 x 10(-9) M), or pirenzepine (4.7 x 10(-7) M), but were blocked completely by atropine (2.92 x 10(-9) M). A significant increase in propulsion of gastrointestinal motility was observed. Acetylcholine, KCl and ID produced contractions in Ca(2+) free media. The phasic components of the contractile responses to Ach as well as the tonic component of K(+) and ID-induced contractions were relatively resistant to short periods of calcium-free exposure. Ach, K(+) and ID still caused contractions in the presence of verapamil. The data revealed that ID-induced contractions were not mediated by histaminergic receptors, calcium channels, M1 muscarinic receptors. It also suggests that Ach mobilize Ca from some tightly bound or intracellular pool, whereas high K(+) and ID may mobilize Ca from some superficial or loosely-bound pool.
研究了木蓝叶水提取物(ID)对小鼠胃肠动力以及从大鼠和豚鼠获得的离体平滑肌制剂的收缩作用。在暴露于无钙缓冲液或生理溶液的大鼠回肠平滑肌上,测量了10^(-6) M乙酰胆碱、80 mM氯化钾和1.6 mg/ml ID的收缩作用,以确定提取物动员用于激活收缩的钙库。还对小鼠进行了急性毒性试验(LD50)。结果表明,ID(0.05 - 3.2 mg/ml)可引起豚鼠和大鼠回肠浓度依赖性收缩。这些反应不受美吡拉敏(2.49×10^(-9) M)、维拉帕米(8.14×10^(-9) M)或哌仑西平(4.7×10^(-7) M)的阻断,但被阿托品(2.92×10^(-9) M)完全阻断。观察到胃肠动力推进显著增加。乙酰胆碱、氯化钾和ID在无钙培养基中产生收缩。对乙酰胆碱收缩反应的相成分以及钾离子和ID诱导收缩的张力成分对短时间无钙暴露相对抗性。在维拉帕米存在的情况下,乙酰胆碱、钾离子和ID仍引起收缩。数据显示,ID诱导的收缩不是由组胺能受体、钙通道、M1毒蕈碱受体介导的。这也表明,乙酰胆碱从一些紧密结合或细胞内钙库中动员钙,而高钾离子和ID可能从一些表面或松散结合的钙库中动员钙。