硫化和氧化改善功能和α-上腺素反应在老鼠的左心室缩
Tabinda Fatima1, Latifah Al Shammari1, Mohamed Ibrahim Lazhari2
1Department of Pharmaceutical Chemistry, College of Pharmacy, University of Hafr Al Batin, Hafr Al Batin 39524, Saudi Arabia.
Current issues in molecular biology
|October 28, 2025
概括
结合硫化 (H2S) 和氧化 (NO) 疗法通过增强皮质血流和上腺受体功能,主要通过ENOS/NO通路,逆转左心室缩 (LVH).
科学领域:
- 心血管生理学心血管生理学
- 脏生理学 脏生理学
- 药理学 药理学 是一个学科.
背景情况:
- 左心室缩 (LVH) 损害功能并改变上腺素受体活性.
- 硫化 (H2S) 和氧化 (NO) 单独改善脏参数和血管反应.
- H2S和NO对LVH诱导的功能障碍的联合作用尚未完全理解.
研究的目的:
- 为了研究H2S和NO联合给药对皮皮质血流 (RCBP) 和阿尔法-上腺素受体响应在LVH的老鼠模型的影响.
- 阐明涉及联合H2S和NO的治疗作用的潜在途径 (eNOS/NO和CSE/H2S).
主要方法:
- 在老鼠中使用咖啡因和异上腺素诱导LVH.
- 大鼠接受了L-氨酸作为一个NO捐赠者,与H2S的管理一起.
- 对上腺激素激动剂的血管反应在与α1-adrenoceptor对抗剂阻塞之前和之后被评估.
- 对CSE和eNOS的脏mRNA表达量化.
主要成果:
- 在LVH大鼠中,联合H2S+NO疗法显著上调脏CSE和eNOSmRNA.
- 与对照组相比,在接受H2S+NO治疗的LVH大鼠中,RCBP显著增加.
- H2S+NO的使用增强了α1A,α1B和α1D上腺素受体的活性,调解血管收缩,即使受体受阻.
结论:
- 同时对H2S和NO捐赠者的外源施用改善了RCBP,功能和LVH大鼠的α1-上腺素受体响应.
- 治疗效果主要通过内皮氧化合成酶 (eNOS) /NO通路进行介导,其中部分贡献来自氨酸γ-酶 (CSE) /H2S通路.
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