Department of Physiology and Pharmacology, Brazilian Semi-Arid Institute of Biomedicine, Faculty of Medicine, Federal University of Ceará, Fortaleza 60430-270, Brazil.
World J Gastroenterol. 2012 Jul 7;18(25):3207-14. doi: 10.3748/wjg.v18.i25.3207.
To investigate the effects of mangiferin on gastrointestinal transit (GIT) in normal and constipated mice, together with the possible mechanism.
Intragastrically-administered charcoal meal was used to measure GIT in overnight starved Swiss mice. In the first experiments, mangiferin (3 mg/kg, 10 mg/kg, 30 mg/kg, and 100 mg/kg, po) or tegaserod (1 mg/kg, ip) were administered 30 min before the charcoal meal to study their effects on normal transit. In the second series, mangiferin (30 mg/kg) was tested on delayed GIT induced by several different pharmacological agonists (morphine, clonidine, capsaicin) or antagonists (ondansetron, verapamil, and atropine) whereas in the third series, mangiferin (30 mg/kg, 100 mg/kg and 300 mg/kg) or tegaserod (1 mg/kg) were tested on 6 h fecal pellets outputted by freely fed mice. The ratio of wet to dry weight was calculated and used as a marker of fecal water content.
Mangiferin administered orally significantly (P < 0.05) accelerated GIT at 30 mg/kg and 100 mg/kg (89% and 93%, respectively), similarly to 5-hydroxytryptamine(4) (5-HT(4)) agonist tegaserod (81%) when compared to vehicle-treated control (63%). Co-administered mangiferin (30 mg/kg) totally reversed the inhibitory effect of opioid agonist morphine, 5-HT(3)-receptor antagonist ondansetron and transient receptor potential vanilloid-1 receptor agonist capsaicin on GIT, but only to a partial extent with the GIT-delay induced by α(2)-adrenoceptor agonist clonidine, and calcium antagonist verapamil. However, co-administered atropine completely blocked the stimulant effect of mangiferin on GIT, suggesting the involvement of muscarinic acetylcholine receptor activation. Although mangiferin significantly enhanced the 6 h fecal output at higher doses (245.5 ± 10.43 mg vs 161.9 ± 10.82 mg and 227.1 ± 20.11 mg vs 161.9 ± 10.82 mg of vehicle-treated control, at 30 and 100 mg/kg, P < 0.05, respectively), the effect of tegaserod was more potent (297.4 ± 7.42 mg vs 161.9 ± 10.82 mg of vehicle-treated control, P < 0.05). Unlike tegaserod, which showed an enhanced water content in fecal pellets (59.20% ± 1.09% vs 51.44% ± 1.19% of control, P < 0.05), mangiferin evidenced no such effect, indicating that it has only a motor and not a secretomotor effect.
Our data indicate the prokinetic action of mangiferin. It can stimulate the normal GIT and also overcome the drug-induced transit delay, via a cholinergic physiological mechanism.
研究芒果苷对正常和便秘小鼠胃肠道转运（GIT）的影响及其可能的机制。
使用隔夜禁食的瑞士小鼠胃内给予炭末来测量 GIT。在第一个实验中，在给予炭末前 30 分钟给予芒果苷（3 mg/kg、10 mg/kg、30 mg/kg 和 100 mg/kg，po）或替加色罗（1 mg/kg，ip），以研究它们对正常转运的影响。在第二个系列中，测试芒果苷（30 mg/kg）对几种不同的药理学激动剂（吗啡、可乐定、辣椒素）或拮抗剂（昂丹司琼、维拉帕米、阿托品）引起的延迟 GIT 的影响，而在第三个系列中，测试芒果苷（30 mg/kg、100 mg/kg 和 300 mg/kg）或替加色罗（1 mg/kg）对自由喂养小鼠 6 小时粪便颗粒的排出量的影响。计算湿重与干重的比值，用作粪便含水量的标志物。
口服给予芒果苷在 30 mg/kg 和 100 mg/kg 时可显著（P<0.05）加速 GIT（分别为 89%和 93%），与 5-羟色胺（4）（5-HT（4））激动剂替加色罗（81%）相似，而与给予载体的对照（63%）相比。给予共芒果苷（30 mg/kg）完全逆转了阿片类激动剂吗啡、5-HT（3）受体拮抗剂昂丹司琼和瞬时受体电位香草酸 1 型受体激动剂辣椒素对 GIT 的抑制作用，但对 α（2）-肾上腺素能受体激动剂可乐定和钙拮抗剂维拉帕米引起的 GIT 延迟仅部分逆转。然而，给予阿托品完全阻断了芒果苷对 GIT 的刺激作用，表明涉及毒蕈碱乙酰胆碱受体的激活。尽管芒果苷在较高剂量时显著增加了 6 小时粪便排出量（30 和 100 mg/kg 时分别为 245.5±10.43 mg 比 161.9±10.82 mg 和 227.1±20.11 mg 比 161.9±10.82 mg 对照，P<0.05），但替加色罗的效果更为明显（297.4±7.42 mg 比 161.9±10.82 mg 对照，P<0.05）。与替加色罗相比，替加色罗增加了粪便颗粒中的水分含量（59.20%±1.09%比对照的 51.44%±1.19%，P<0.05），而芒果苷则没有这种作用，表明它只有运动作用而没有分泌运动作用。
我们的数据表明芒果苷具有促动力作用。它可以通过胆碱能生理机制刺激正常的 GIT，并且还可以克服药物引起的转运延迟。
