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抑制编程细胞死亡因子4通过减弱双边洞穴神经压伤损伤的老鼠的亡来恢复勃起功能

Yunlong Ge¹, Tian Xia¹, Zejia Feng¹

¹Department of Urology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

|January 13, 2024

概括

减少编程细胞死亡因子4 (PCDCF4) 表达改善了大鼠洞穴神经损伤后的勃起功能障碍. 通过调节PI3K/AKT通路并降低亡,PCDCF4 Knockdown通过调节PI3K/AKT通路并降低亡来提高勃起功能.

科学领域:

泌尿器科泌尿器科泌尿器科泌尿器科
细胞生物学细胞生物学
再生医学是一种再生医学.

背景情况:

根源性前列腺切除术后的勃起功能障碍 (ED) 与亡有关.
编程细胞死亡因子4 (PCDCF4) 影响各种细胞中的细胞亡.
由于洞穴神经损伤导致的ED中PCDCF4的作用仍然不清楚.

研究的目的:

为了研究PCDCF4在双边洞穴神经压碎引起的ED的老鼠模型中的功能.
为了确定PCDCF4是否在神经损伤后的ED病理机制中发挥作用.

主要方法:

雄性Sprague Dawley大鼠经历了双边洞穴神经粉碎或假手术.
编程细胞死亡因子4 (PCDCF4) 表达是使用lentivirus介导的短毛RNA (shRNA) 来调节的.
通过电刺激来评估阴茎勃起功能,随后进行组织学分析和洞穴组织的西部抹迹.

主要成果:

双边洞穴神经被压碎,在大鼠洞穴体中增加了亡和PCDCF4表达.
抑制PCDCF4在受影响的老鼠中显著改善了勃起功能.
通过PI3K/AKT途径介导的PCDCF4敲击增加了光滑肌肉含量,减少了纤维化和减弱的亡.

结论:

过高的PCDCF4表达与洞穴神经损伤后的ED病变有关.
向PCDCF4可以提高勃起功能,并减轻老鼠神经损伤后的亡.
PI3K/AKT通路是PCDCF4影响洞穴性亡的潜在机制.

关键词:

在PDCD4中使用PDCD4.灭症 (apoptosis) 是一种死亡的过程.洞穴神经是一种神经.这是勃起功能障碍.鼠类鼠类鼠类鼠类鼠类

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