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HO-1 cDNA-脂质体复合物转染对老年大鼠勃起信号传导的影响。

Effect of HO-1 cDNA-liposome complex transfer on erectile signalling of aged rats.

作者信息

Abdel Aziz M T, Mostafa T, Atta H, Mahfouz S, Wassef M, Fouad H, Kamel M, Rashed L, Sabry D, Mouhamed O

机构信息

Department of Medical Biochemistry, Faculty of Medicine, Cairo University, Cairo, Egypt.

出版信息

Andrologia. 2009 Jun;41(3):176-83. doi: 10.1111/j.1439-0272.2008.00911.x.

Abstract

This work aimed to assess the efficacy of haeme oxygenase-1 (HO-1) cDNA-liposome complex transfer as a mediator of erectile signalling in aged rats. One hundred and fifty aged white albino rats were equally divided into five groups: controls, rats receiving lipofectamine, rats receiving intracorporeal HO-1 cDNA-lipsome complex, rats receiving HO-1 cDNA-liposome complex plus nitric oxide synthase (NOS) inhibitor, and rats receiving HO-1 cDNA-liposome complex plus HO inhibitor. Six rats were killed from each group after 12, 24 and 48 h, and after1 and 2 weeks. In dissected cavernous tissues, the following were assessed: HO-1 gene expression, Western blot for HO-1, HO enzyme activity, cGMP and histopathology. The results showed that HO-1 cDNA-liposome complex transfer led to a significant increase in cavernous tissue HO-1 protein, HO-1 gene expression, HO enzyme activity and cGMP up to 1 week. NOS inhibition exhibited no effect on HO-1 gene enhancement of cavernous tissue HO enzyme activity or cGMP, whereas inhibition of HO significantly decreased these parameters. Histopathology of cavernous tissue demonstrated a significant dilatation of helicine arteries in HO-1 cDNA-liposome complex treated group after 48 h compared with the controls. It is concluded that HO-1 cDNA-liposome complex transfer augments cavernous tissue cGMP with subsequent sinusoidal relaxation.

摘要

这项研究旨在评估血红素加氧酶-1(HO-1)cDNA-脂质体复合物转移作为老年大鼠勃起信号传导介质的功效。150只老年白色白化病大鼠被平均分为五组:对照组、接受脂质体转染试剂的大鼠、接受体内HO-1 cDNA-脂质体复合物的大鼠、接受HO-1 cDNA-脂质体复合物加一氧化氮合酶(NOS)抑制剂的大鼠以及接受HO-1 cDNA-脂质体复合物加HO抑制剂的大鼠。在12、24和48小时以及1周和2周后,每组处死6只大鼠。在解剖的海绵体组织中,评估以下指标:HO-1基因表达、HO-1的蛋白质免疫印迹、HO酶活性、环磷酸鸟苷(cGMP)和组织病理学。结果表明,HO-1 cDNA-脂质体复合物转移导致海绵体组织HO-1蛋白、HO-1基因表达、HO酶活性和cGMP显著增加,持续长达1周。抑制NOS对海绵体组织HO酶活性或cGMP的HO-1基因增强无影响,而抑制HO则显著降低这些参数。与对照组相比,48小时后,HO-1 cDNA-脂质体复合物处理组海绵体组织的组织病理学显示螺旋动脉明显扩张。得出的结论是,HO-1 cDNA-脂质体复合物转移可增加海绵体组织cGMP,随后导致海绵体窦状隙松弛。

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