阿皮拉尼尔通过调节亡和氧化应激来减轻帕拉西托醇诱导的肝毒性
Nurcan Bıçakçı1, İhsan Karaboğa2, Sercan Bıçakçı3
1Emergency and Disaster Management Department, Tekirdag Namık Kemal University, Faculty of Health Sciences, Tekirdag, Türkiye.
概括
蜜蜂产品阿皮拉尼尔 (AP) 显示出治疗性作用,可以预防类醇诱导的肝损伤. 通过减少氧化应激和调节与亡相关的蛋白质表达,AP治疗减轻了肝毒性.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 药理学 药理学是指药理学的学科.
- 毒理学 毒理学 毒理学
背景情况:
- 偏醇 (PAR) 是一种广泛使用的止痛药,对肝毒性的治疗选择有限.
- 阿皮拉尼尔 (AP) 是一种富含多的蜜蜂产品,具有显著的抗氧化特性.
- 以前的研究表明,AP可以保护肝脏免受其他毒素的损伤,但其在PAR诱导的肝毒性中的作用尚未被探索.
研究的目的:
- 调查阿皮拉尼尔 (AP) 在减轻类醇 (PAR) 诱导的肝毒性方面的治疗潜力.
- 在PAR诱导的肝损伤模型中探索AP治疗,氧化应激和亡之间的关系.
主要方法:
- 一个实验性体内模型被用来诱导肝毒性与甲醇 (PAR).
- 评估了阿皮拉尼尔 (AP) 治疗对肝脏组织病理学的影响.
- 评估了亡 (p53,caspase-3) 和氧化压力的关键标志物 (马隆迪甲,甲基酶,谷氨过氧化酶).
主要成果:
- 降醇的使用引发了严重的肝损伤,其特征是肝细胞结构的改变,鼻状变化和炎症.
- PAR治疗增加了p53和caspase-3表达和malondialdehyde (MDA) 水平,同时降低了catalase (CAT) 和glutathione peroxidase (GSHpx) 的水平.
- 阿皮拉尼尔 (AP) 治疗显著改善了肝脏组织病理学,并减少了p53和caspase-3的表达.
结论:
- 阿皮拉尼尔 (AP) 显示出显著的治疗疗效,可以缓解类醇诱导的肝毒性.
- 通过调节氧化应激路径和调节与亡相关的蛋白质表达,特别是p53和caspase-3来发挥其保护作用.
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