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S-和R-卡维迪洛尔防止子烯诱导的肺癌发生

Ayaz Shahid¹, Steven Yeung¹, Bradley T Andresen¹

¹Department of Biotechnology and Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, California, USA.

Thoracic cancer

|June 19, 2025

概括

卡维迪洛尔通过独立于其β-阻断剂活性的机制预防由甲烯 (B) 引起的肺癌. 在小鼠中,S-和R-carvedilol异构体都有效抑制了B(a) P诱导的肺炎和瘤发育.

科学领域:

药理学药理学是指药理学的学科.
在瘤学瘤学.
毒理学毒理学毒理学

背景情况:

肺癌仍然是癌症相关死亡的主要原因.
卡维迪洛尔是一种β-阻断剂,此前已证明其在预防酸[B]诱导的肺癌方面具有有效性.
卡尔维迪醇是一种含有S-卡尔维迪醇 (β-上腺素阻断剂) 和R-卡尔维迪醇 (缺乏β-阻断活性) 的种族混合物.

研究的目的:

调查卡维迪洛的肺癌预防作用是否通过其β-阻断活性进行中介.
为了比较S-和R-carvedilol在预防由B(a) P及其代谢物,二烯二醇环氧化物 (BPDE) 诱导的肺癌方面的疗效.

主要方法:

在体外研究中使用暴露于BPDE的人类支气管上皮细胞系BEAS-2B.
在体内研究中,小鼠暴露于B(a) P,并给予S-或R-carvedilol.
评估细胞转化,阿里碳化合物受体 (AhR) /外源生物反应元素 (XRE) 激活,CYP1A1 mRNA表达,炎症标志物和瘤发育.

主要成果:

无论是S-和R-carvedilol都同样防止了BEAS-2B细胞的BPDE诱导的恶性转变.
这两种异构体都抑制了B(a) P诱导的AhR/XRE激活和CYP1A1mRNA在BEAS-2B细胞中的表达.
在小鼠中,S-和R-carvedilol显著降低了B(a) P诱导的肺炎,氧化应激标志物 (乳酸脱酶,马隆迪化物) 和基因病学损伤.
用S-或R-carvedilol治疗显著减少了暴露于B(a) P的小鼠肺部瘤的数量和大小.

结论:

卡维迪洛尔通过独立于其β-阻断活性的机制预防B(a) P诱导的肺炎和致癌症.
两种S-和R-carvedilol异构体在预防肺癌发展方面表现出相似的疗效.
这些发现表明R-carvedilol缺乏β-阻断活性,可能具有预防肺癌的治疗潜力.

关键词:

这是一种R-carvedilol.子甲烯 (a) 烯化学预防化学预防肺癌是一种肺癌.烟草吸烟吸烟烟草吸烟在β-Blockaders中使用.

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