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cAMP化酶抑制剂通过调节二甲基氨酸二甲基氨基酸酶来增加氧化的产生

Soni Savai Pullamsetti¹, Rajkumar Savai, Martina Barbara Schaefer

¹Max-Planck-Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany.

|March 9, 2011

概括

联合PDE3和4抑制通过调节ADMA-DDAH轴来改善肺高血压中的内皮功能. 这种方法减少了亡并促进了血管再生,提供了一种新的治疗策略.

科学领域:

心血管研究研究心血管研究
肺高血压的病理生理学
内皮细胞生物学内皮细胞生物学

背景情况:

肺动脉高血压包括内皮功能障碍,血管重塑和肺血管损失.
不对称的二甲基氨基 (ADMA) 和其代谢酶DDAH是内皮功能障碍的关键因素.
研究固酶 (PDE) 3和4抑制在ADMA-DDAH轴调节中的作用至关重要.

研究的目的:

通过调节ADMA-DDAH轴,研究联合PDE3和4抑制是否可以改善内皮功能.
探索PDE3/4抑制剂对内皮细胞和肺高血压的小鼠模型的影响.

主要方法:

在体外对内皮细胞的研究评估了生存,增殖,亡,氧化通路,DDAH表达和促进体活性.
在体内研究中,在老鼠中使用单克罗他林诱导的肺高血压,与吸入PDE3/4抑制剂治疗.
技术包括实时PCR,免疫细胞化学,PDE活性测定和血液动力学/气体交换测量.

主要成果:

抑制PDE3/4通过诱导DDAH2.2,通过cAMP/PKA依赖的途径减少了ADMA诱导的亡.
吸入PDE3/4抑制剂在老鼠中减轻了血液动力学异常,血管重塑和右心脏缩.
治疗减少了ADMA,增加了氧化/cGMP水平,抑制了内皮细胞亡,并增强了肺血管化.

结论:

结合PDE3和4抑制有效逆转肺高血压的发展.
这种治疗策略通过调节ADMA-DDAH轴来促进内皮再生.
准PDE3/4为治疗肺高血压提供了一个有希望的方法.

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