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为探索雌二醇(E2)对应激性胃溃疡发生的影响及机制,以电剌激束缚雄性小鼠口唇部1h诱发胃溃疡,用阿尔新兰—氯化镁洗脱法测定胃壁粘蛋白。结果表明,肌肉注射(im)E244μg·kg-1后1h电刺激束缚应激(ERS)或imE2176μg·kg-1后立即ERS可明显加剧胃溃疡,并使胃壁粘蛋白量显著减少。侧脑室注射非惊厥剂量(0.08μg/5μl/只)印防己毒素(Pic)或惊厥剂量(0.3μg/5μl/只)均可完全消除E2的加剧效应,安定、异丙肾上腺素和阿托品都不能影响E2的加剧效应。表明外源性E2进入体内后可削弱胃粘液屏障,加剧电刺激束缚应激胃溃疡,此效应可能是E2随血液循环透过血—脑屏障,通过作用脑中GABAA受体实现的
To explore the effect and mechanism of estradiol (E2) on gastric ulcer induced by gastric ulcer, gastric ulcer was induced by electrical stimulation for 1 h on the lips of male mice, and gastric mucin was detected by Alcian blue-chloride elution method. The results showed that ERS immediately after stimulation with restraint stress (ERS) or imE2176μg · kg-1 at 1h after intramuscular injection of E244μg · kg-1 could significantly aggravate gastric ulcer and significantly decrease gastric mucin content. Intracerebroventricular injection of non-convulsive dose (0.08 μg / 5 μl / only) picrotoxin (Pic) or convulsant dose (0.3 μg / 5 μl / only) can completely eliminate the exacerbating effect of E2, diazepam, isoproterenol and atropine can not Affect the exacerbating effect of E2. It is suggested that exogenous E2 can weaken the gastric mucosal barrier and aggravate the irritation of stomach ulcer by electrical stimulation. This effect may be caused by the action of E2 through the blood-brain barrier with the blood circulation through the action of GABAA receptor in the brain