Lupeol (1) was isolated from hexane branch extract of Maytenus salicifolia and the Lupeol stearate (2), Lupeol palmitate (3), Lupeol myristate (4), Lupeol laurate (5) and Lupeol caprylate (6) were obtained reacting 1 with an adequate carboxylic acid. Swiss mice were treated with vehicle, carbenoxolone or Lupeol esters before administration of ethanol/HCl or indomethacin. Additionally, the involvement of nitric oxide (NO), sulfhydryl compounds (NP-SH), α-2 adrenergic receptors (α2-AR) and prostaglandins (PGE) in antiulcer effects was investigated using appropriate inhibitors or antagonist. Oxidative and inflammatory parameters were measured after euthanasia and anti-secretory effects was evaluated in pylorus-ligated rats. Ethanol/HCl ulcerated the gastric mucosa by 64.45 ± 6.58 mm2, which the oral treatment with 1, 4 and 6 (10 mg/kg), and 3 and 5 (30 mg/kg) reduced the lesion area. Interestingly, 2 reduced the gastric ulcer by oral route in a potent and dose-dependent manner (ED50 = 0.40 mg/kg), which was accompanied by the increase in reduced glutathione levels and by the reduction of lipids peroxidation and myeloperoxidase and superoxide dismutase activities. Moreover, 2 (0.1 mg/kg) also prevented the ulcerogenesis by intraperitoneal route. The participation of NO, NP-SH, α2-AR and PGE in 2-mediated gastroprotection was confirmed. In indomethacin-induced ulcer, 2 (1 mg/kg, p.o) also reduced the ulcer area and increased the PGE2 levels. However, 2 did not alter the gastric acid secretion. Therefore, these findings indicate that the obtention of 2 potentiated the antiulcer activity of 1 and that this compound can elicit gastroprotective action due a diversified mode of action.

中文翻译：

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Lupeol衍生酯的胃保护特性：Lupeol-stearate作为强效抗溃疡药的临床前证据。

从美登（的己烷分支提取物中分离出Lupeol（1），并获得Lupeol硬脂酸酯（2），Lupeol棕榈酸酯（3），Lupeol肉豆蔻酸酯（4），Lupeol月桂酸酯（5）和Lupeol辛酸酯（6），使1与足够的羧酸。在给予乙醇/ HCl或消炎痛之前，先用赋形剂，羧甲基环己酮或Lupeol酯治疗瑞士小鼠。此外，使用适当的抑制剂或拮抗剂研究了一氧化氮（NO），巯基化合物（NP-SH），α-2肾上腺素能受体（α2-AR）和前列腺素（PGE）在抗溃疡作用中的作用。安乐死后测量氧化和炎症参数，并在幽门结扎的大鼠中评估其抗分泌作用。乙醇/ HCl可使胃黏膜溃疡64.45±6.58 mm2，口服，1、4和6（10 mg / kg）口服治疗，3和5（30 mg / kg）减少了病变面积。有趣的是，2通过口服途径以有效且剂量依赖性的方式减少了胃溃疡（ED50 = 0.40 mg / kg），这伴随着谷胱甘肽水平降低的增加以及脂质过氧化，髓过氧化物酶和超氧化物歧化酶活性的降低。 。此外，2（0.1 mg / kg）也可通过腹膜内途径预防溃疡发生。证实了NO，NP-SH，α2-AR和PGE参与了2-介导的胃保护。在吲哚美辛诱发的溃疡中，2（1 mg / kg，po）也可减少溃疡面积并增加PGE2水平。但是，2并没有改变胃酸的分泌。因此，这些发现表明获得2增强了1的抗溃疡活性，并且该化合物由于作用方式多样而可以引起胃保护作用。