研究动态
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(-)-Fenchone 可通过抗氧化和免疫调节机制预防半胱胺诱发的十二指肠溃疡并加速愈合,促进大鼠胃溃疡的再上皮化。

(-)-Fenchone Prevents Cysteamine-Induced Duodenal Ulcers and Accelerates Healing Promoting Re-Epithelialization of Gastric Ulcers in Rats via Antioxidant and Immunomodulatory Mechanisms.

发表日期:2024 May 15
作者: Maria Elaine Cristina Araruna, Edvaldo Balbino Alves Júnior, Catarina Alves de Lima Serafim, Matheus Marley Bezerra Pessoa, Michelle Liz de Souza Pessôa, Vitória Pereira Alves, Marcelo Sobral da Silva, Marianna Vieira Sobral, Adriano Francisco Alves, Mayara Karla Dos Santos Nunes, Aurigena Antunes Araújo, Leônia Maria Batista
来源: HEART & LUNG

摘要:

(-)-Fenchone 是一种天然存在的单萜,存在于茴香 (Foeniculum vulgare Mill.)、侧柏 (Thuja occidentalis L.) 和白马 (Peumus Boldus Molina) 的精油中。药理学研究报道了其镇痛、抗菌、抗炎、止泻和抗氧化活性。(-)-小茴香酮的预防性抗溃疡作用通过半胱胺诱导的十二指肠病变模型的口服预处理进行了评估。使用口服治疗 14 天的乙酸诱导的胃溃疡大鼠模型评估重复给药后的胃愈合、潜在机制和毒性。在半胱胺诱导的十二指肠溃疡模型中,小茴香酮(37.5-300 mg/kg)显着减少溃疡面积并防止病变形成。在乙酸诱导的溃疡模型中,小茴香酮 (150 mg/kg) 可减少 (p < 0.001) 溃疡损伤。这些影响与还原型谷胱甘肽 (GSH)、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) 水平的增加有关。此外,(-)-Fenchone (150 mg/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 1 β (IL-1β)、肿瘤坏死因子 α (TNF-) α) 和核转录因子 kappa B (NF-κB)。 14 天的口服毒性调查显示,心脏、肝脏、脾脏或肾脏重量以及所评估的生化和血液学参数均未发生变化。 (-)-小茴香酮可保护动物免于体重减轻,同时保持饲料和水的摄入量。(-)-小茴香酮毒性低,可预防十二指肠溃疡,并增强胃愈合活性。抗氧化和免疫调节特性似乎与其治疗作用有关。
(-)-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.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.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.(-)-Fenchone exhibits low toxicity, prevents duodenal ulcers, and enhances gastric healing activities. Antioxidant and immunomodulatory properties appear to be involved in its therapeutic effects.