Olaleye S B, Farombi E O
Department of Physiology, College of Medicine, University of Ibadan, Nigeria.
Phytother Res. 2006 Jan;20(1):14-20. doi: 10.1002/ptr.1793.
Reactive oxygen species (ROS) have been implicated in the aetiology of HCl/ethanol- and indomethacin gastric mucosal damage. This study investigated the protective effects of kolaviron, a natural antioxidant from the seed of Garcinia kola, on oxidative gastric mucosal damage induced by HCl/ethanol, and indomethacin.A HCl/ethanol mixture (1.5 mL of 0.15 n HCl in 70% ethanol) and indomethacin (IND) caused severe gastric damage with an ulcer index of 2.90 +/- 0.8 and 2.5 +/- 0.4, respectively, and significant reductions in the gastric mucosal content of catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) (p < 0.001).Pre-treatment of animals with kolaviron (100 mg/kg) orally 1 h and once daily for 3 days prior to ulcer induction significantly reduced the formation of ulcers induced by HCl/ethanol with preventive ratios of 65 and 72, respectively, while rats treated with kolaviron 1 day and for 7 days prior to IND treatment attenuated ulcer formation by 59% and 77%. Pre-treatment with ranitidine 1 h prior to ulcer induction (50 mg/kg) elicited preventive ulcer ratio of 55. Kolaviron pre-treatment 1 h before ulcer induction attenuated the HCl/ethanol reduction in CAT, SOD and GSH by 43%, 42% and 30%, respectively, and 67%, 68% and 64% following 72 h treatment with kolaviron. Ranitidine elicited 24%, 41% and 29% protective effects, respectively.Similarly, kolaviron administered to rats 1 day and for 7 days before IND treatment attenuated the drug-induced inhibition of CAT by 44% and 70%; SOD by 23% and 43% and GSH by 32% and 55%, respectively. In a 1 h and 3-day treatment with kolaviron before HCl/ethanol administration, MDA was reduced by 35% and 55%, respectively, while kolaviron administration 1 day and for 7 days before IND elicited a 39% and 58% reduction in MDA. Ranitidine elicited 39% and 50% reduction in MDA following HCl/ethanol and IND treatment. The results indicate the gastroprotective activity of kolaviron, which may be linked to its intrinsic antioxidant properties.
活性氧（ROS）与盐酸/乙醇和吲哚美辛所致胃黏膜损伤的病因有关。本研究调查了可乐维隆（一种来自可乐果种子的天然抗氧化剂）对盐酸/乙醇和吲哚美辛诱导的氧化性胃黏膜损伤的保护作用。盐酸/乙醇混合物（1.5 mL 0.15 n盐酸溶于70%乙醇中）和吲哚美辛（IND）分别导致严重的胃损伤，溃疡指数分别为2.90±0.8和2.5±0.4，同时胃黏膜中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽（GSH）的含量显著降低（p<0.001）。在诱导溃疡前1小时口服可乐维隆（100 mg/kg）并连续3天每天给药一次，可显著减少盐酸/乙醇诱导的溃疡形成，预防率分别为65%和72%，而在IND治疗前1天和7天用可乐维隆治疗的大鼠溃疡形成分别减轻了59%和77%。在诱导溃疡前1小时用雷尼替丁（50 mg/kg）预处理，预防溃疡率为55%。在诱导溃疡前1小时用可乐维隆预处理可使盐酸/乙醇所致的CAT、SOD和GSH降低分别减轻43%、42%和30%，用可乐维隆治疗72小时后分别减轻67%、68%和64%。雷尼替丁的保护作用分别为24%、41%和29%。同样，在IND治疗前1天和7天给大鼠服用可乐维隆可使药物诱导的CAT抑制分别减轻44%和70%；SOD抑制分别减轻23%和43%，GSH抑制分别减轻32%和55%。在给予盐酸/乙醇前1小时和3天用可乐维隆治疗，丙二醛（MDA）分别降低35%和55%，而在IND治疗前1天和7天用可乐维隆治疗，MDA分别降低39%和58%。雷尼替丁在盐酸/乙醇和IND治疗后使MDA分别降低39%和50%。结果表明可乐维隆具有胃保护活性，这可能与其内在的抗氧化特性有关。
