PDF(Pubmed)
Abstract：
BACKGROUND: (-)-Fenchone is a naturally occurring monoterpene found in the essential oils of Foeniculum vulgare Mill., Thuja occidentalis L., and Peumus boldus Molina. Pharmacological studies have reported its antinociceptive, antimicrobial, anti-inflammatory, antidiarrheal, and antioxidant activities.
METHODS: The preventive antiulcer effects of (-)-Fenchone were assessed through oral pretreatment in cysteamine-induced duodenal lesion models. Gastric healing, the underlying mechanisms, and toxicity after repeated doses were evaluated using the acetic acid-induced gastric ulcer rat model with oral treatment administered for 14 days.
RESULTS: In the cysteamine-induced duodenal ulcer model, fenchone (37.5-300 mg/kg) significantly decreased the ulcer area and prevented lesion formation. In the acetic acid-induced ulcer model, fenchone (150 mg/kg) reduced (p < 0.001) ulcerative injury. These effects were associated with increased levels of reduced glutathione (GSH), superoxide dismutase (SOD), interleukin (IL)-10, and transforming growth factor-beta (TGF-β). Furthermore, treatment with (-)-Fenchone (150 mg/kg) significantly reduced (p < 0.001) malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and nuclear transcription factor kappa B (NF-κB). A 14-day oral toxicity investigation revealed no alterations in heart, liver, spleen, or kidney weight, nor in the biochemical and hematological parameters assessed. (-)-Fenchone protected animals from body weight loss while maintaining feed and water intake.
CONCLUSIONS: (-)-Fenchone exhibits low toxicity, prevents duodenal ulcers, and enhances gastric healing activities. Antioxidant and immunomodulatory properties appear to be involved in its therapeutic effects.
METHODS: The preventive antiulcer effects of (-)-Fenchone were assessed through oral pretreatment in cysteamine-induced duodenal lesion models. Gastric healing, the underlying mechanisms, and toxicity after repeated doses were evaluated using the acetic acid-induced gastric ulcer rat model with oral treatment administered for 14 days.
RESULTS: In the cysteamine-induced duodenal ulcer model, fenchone (37.5-300 mg/kg) significantly decreased the ulcer area and prevented lesion formation. In the acetic acid-induced ulcer model, fenchone (150 mg/kg) reduced (p < 0.001) ulcerative injury. These effects were associated with increased levels of reduced glutathione (GSH), superoxide dismutase (SOD), interleukin (IL)-10, and transforming growth factor-beta (TGF-β). Furthermore, treatment with (-)-Fenchone (150 mg/kg) significantly reduced (p < 0.001) malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and nuclear transcription factor kappa B (NF-κB). A 14-day oral toxicity investigation revealed no alterations in heart, liver, spleen, or kidney weight, nor in the biochemical and hematological parameters assessed. (-)-Fenchone protected animals from body weight loss while maintaining feed and water intake.
CONCLUSIONS: (-)-Fenchone exhibits low toxicity, prevents duodenal ulcers, and enhances gastric healing activities. Antioxidant and immunomodulatory properties appear to be involved in its therapeutic effects.
摘要：
背景：（-）-Fenchone是一种天然存在的单萜，存在于FoeniculumvulgareMill的精油中。,刺槐L.，和PeumusboldusMolina.药理学研究报告了它的抗伤害感受，抗菌，抗炎,止泻药,和抗氧化活性。
方法：通过口服预处理在半胱胺诱导的十二指肠损伤模型中评估（-）-芬酮的预防性抗溃疡作用。胃愈合，潜在的机制，使用口服给药14天的乙酸诱导的胃溃疡大鼠模型评估重复给药后的毒性。
结果：在半胱胺诱导的十二指肠溃疡模型中，芬酮（37.5-300mg/kg）显着减少了溃疡面积并防止了病变的形成。在乙酸诱导的溃疡模型中，芬局酮（150mg/kg）减轻（p<0.001）溃疡性损伤。这些影响与还原型谷胱甘肽（GSH）水平升高有关，超氧化物歧化酶（SOD），白细胞介素（IL）-10和转化生长因子-β（TGF-β）。此外，用（-）-Fenchone（150mg/kg）治疗显着降低（p<0.001）丙二醛（MDA），髓过氧化物酶(MPO),白细胞介素-1β（IL-1β），肿瘤坏死因子-α（TNF-α），核转录因子κB(NF-κB)。一项为期14天的口服毒性研究显示心脏没有改变，肝脏,脾,脾或肾脏重量，在评估的生化和血液学参数中也没有。（-）-Fenchone保护动物免受体重减轻，同时保持饲料和水的摄入量。
结论：（-）-芬酮具有低毒性，预防十二指肠溃疡,并增强胃愈合活动。抗氧化和免疫调节特性似乎涉及其治疗效果。
方法：通过口服预处理在半胱胺诱导的十二指肠损伤模型中评估（-）-芬酮的预防性抗溃疡作用。胃愈合，潜在的机制，使用口服给药14天的乙酸诱导的胃溃疡大鼠模型评估重复给药后的毒性。
结果：在半胱胺诱导的十二指肠溃疡模型中，芬酮（37.5-300mg/kg）显着减少了溃疡面积并防止了病变的形成。在乙酸诱导的溃疡模型中，芬局酮（150mg/kg）减轻（p<0.001）溃疡性损伤。这些影响与还原型谷胱甘肽（GSH）水平升高有关，超氧化物歧化酶（SOD），白细胞介素（IL）-10和转化生长因子-β（TGF-β）。此外，用（-）-Fenchone（150mg/kg）治疗显着降低（p<0.001）丙二醛（MDA），髓过氧化物酶(MPO),白细胞介素-1β（IL-1β），肿瘤坏死因子-α（TNF-α），核转录因子κB(NF-κB)。一项为期14天的口服毒性研究显示心脏没有改变，肝脏,脾,脾或肾脏重量，在评估的生化和血液学参数中也没有。（-）-Fenchone保护动物免受体重减轻，同时保持饲料和水的摄入量。
结论：（-）-芬酮具有低毒性，预防十二指肠溃疡,并增强胃愈合活动。抗氧化和免疫调节特性似乎涉及其治疗效果。
