维生素B12对大鼠中甲铁酸诱导的心脏毒性的作用
Nurhan Kuloğlu1, Derya Karabulut2, Emin Kaymak3
1Healthcare Services Department, Niğde Ömer Halisdemir University, Nigde, Turkey.
Iranian journal of basic medical sciences
|April 22, 2024
概括
维生素B12通过恢复分子标记物和减少心脏损伤,保护免受甲基酸心脏毒性影响. 建议在甲醇前后补充甲醇,以抵消叶酸枯竭.
科学领域:
- 药理学 药理学是指药理学的学科.
- 毒理学 毒理学 毒理学
- 心血管研究研究心血管研究
背景情况:
- 甲甲酸 (MTX) 是一种具有抗炎和免疫抑制功能的化疗剂.
- MTX作为叶酸抗剂,可能导致心脏毒性.
- 了解MTX诱导心脏毒性的分子机制对于制定保护策略至关重要.
研究的目的:
- 研究MTX诱导心脏毒性背后的分子机制.
- 评估维生素B12对MTX心脏毒性的保护作用.
主要方法:
- 一项涉及32只大鼠的研究分为四组:对照组,维生素B12,MTX和MTX+维生素B12.
- 评估心脏组织标记物,包括缺氧诱导因子1α (HIF1-α),VEGFR-2,EPO,IL-6,催化酶 (CAT),超氧化物转化酶 (SOD) 和恶性甲 (MDA).
- 对血清生物标志物ANP和NT-proBNP的测量.
主要成果:
- 服用MTX导致HIF1-α和VEGFR-2表达增加,IL-6和EPO减少,CAT和SOD减少,MDA水平升高.
- 维生素B12补充剂显著逆转了这些MTX诱导的变化.
- 维生素B12还显著降低了由MTX引起的ANP和NT-proBNP水平的升高.
结论:
- 维生素B12在分子和生物化学水平上显示出对MTX诱导的心脏毒性的显著保护作用.
- 建议在MTX给药前后补充维生素B12,以减轻叶酸枯竭和相关的心脏损伤.
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