Iwasaki Yoshikazu, Matsui Teruaki, Arakawa Yasuyuki
Division of Gastroenterology and Hepatology, Department of Medicine, Nihon University School of Medicine, 30-1 Oyaguchi Kamimachi, Itabashi-ku, 173-8610 Tokyo, Japan.
J Gastroenterol. 2004 Sep;39(9):831-7. doi: 10.1007/s00535-004-1399-5.
Proanthocyanidin, a grape-seed polyphenol, has been reported to have protective properties against vascular injury and ulcers, preventive effects against atherosclerosis and cancer, and antioxidative effects, such as improving lipid metabolism and slowing aging. However, little has been reported on its antiulcer effects. We aimed to elucidate the antiulcer mechanism of proanthocyanidin.
Gravinol, containing 89.3% proanthocyanidin, was used. Proanthocyanidin solution, in distilled water, at 0.002%, 0.02%, 0.2%, or 1%, was given to rats ad libitum for 2 weeks. Distilled water was given to control rats. The effect of proanthocyanidin on gastric mucosal injury was investigated with the water-immersion restraint stress model. The ratios of areas of hemorrhagic erosion were compared as the lesion index. Myeloperoxidase activities were also examined, as an index of tissue injury. Superoxide dismutase activity was measured to examine its antioxidative effect. Furthermore, serum gastrin, somatostatin, histamine, and prostaglandin E(2) levels were measured in this rat model.
Proanthocyanidin administration significantly suppressed gastric mucosal injury, induced by water-immersion restraint stress, in a dose-dependent manner. Myeloperoxidase activities were also significantly inhibited, whereas superoxide dismutase activities were significantly stimulated. As to gastrointestinal hormones, the secretion of gastrin, somatostatin, and histamine was significantly inhibited, while prostaglandin E(2) secretion was significantly stimulated.
Proanthocyanidin was shown to have a protective effect on the gastric mucosa. The mechanisms underlying the effect of proanthocyanidin were considered to be the following: anti-gastrin and anti-histamine effects to prevent attacks by water-immersion restraint stress, and mucoprotective properties, bestowed by increased prostaglandin and increased superoxide dismutase activities in the gastric mucosa.
原花青素是一种葡萄籽多酚，据报道具有抗血管损伤和溃疡的保护特性、抗动脉粥样硬化和癌症的预防作用以及抗氧化作用，如改善脂质代谢和延缓衰老。然而，关于其抗溃疡作用的报道较少。我们旨在阐明原花青素的抗溃疡机制。
使用含有89.3%原花青素的葡萄籽提取物。将0.002%、0.02%、0.2%或1%的原花青素溶液用蒸馏水配制，随意给予大鼠2周。给予对照大鼠蒸馏水。用水浸束缚应激模型研究原花青素对胃黏膜损伤的影响。比较出血性糜烂面积的比例作为损伤指数。还检测髓过氧化物酶活性作为组织损伤指标。测量超氧化物歧化酶活性以检查其抗氧化作用。此外，在该大鼠模型中测量血清胃泌素、生长抑素、组胺和前列腺素E2水平。
给予原花青素可显著抑制水浸束缚应激诱导的胃黏膜损伤，且呈剂量依赖性。髓过氧化物酶活性也显著受到抑制，而超氧化物歧化酶活性则显著增强。至于胃肠激素，胃泌素、生长抑素和组胺的分泌显著受到抑制，而前列腺素E2分泌则显著增加。
原花青素对胃黏膜具有保护作用。原花青素发挥作用的机制被认为如下：抗胃泌素和抗组胺作用可防止水浸束缚应激的攻击，以及胃黏膜中前列腺素增加和超氧化物歧化酶活性增强所赋予的黏膜保护特性。
