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大鼠动脉中一氧化氮途径的年龄相关变化及脱氢表雄酮的干预作用研究

Research on the age-related changes in the nitric oxide pathway in the arteries of rats and the intervention effect of dehydroepiandrosterone.

作者信息

Wu Saizhu, Ruan Yunjun, Yin Mengzhuo, Lai Wenyan

机构信息

Department of Cardiology, Nanfang Hospital, Guangzhou, China.

出版信息

Gerontology. 2007;53(4):234-7. doi: 10.1159/000100961. Epub 2007 Mar 20.

Abstract

BACKGROUND

Aging, especially the aging of blood vessels, is a dangerous independent factor in the occurrence and development of cardiovascular and cerebrovascular diseases. However, the cellular and molecular pathologic mechanisms underlying the aging of blood vessels remain unclear.

PURPOSE

To observe changes in the nitric oxide (NO) pathway and the interventional effects of dehydroepiandrosterone (DHEA) in the artery during the aging process.

METHODS

Male Wistar rats were divided into 3 experimental groups of 6 rats each: group 1, adult control 12-month-old rats fed conventional fodder; group 2, 18-month-old rats fed conventional fodder, and group 3, 18-month-old rats that received 1 mg/kg/ DHEA in their fundamental fodder when they were 12 months old. The thoracic aorta was chosen. Endothelial NO synthase protein was measured using the Western blot method, the amount of NO using the Griess method, the amount of cGMP using radioimmunoassay, and the activity of superoxide dismutase (SOD) and the amount of malonyldialdehyde (MDA) using colorimetry.

RESULT

Compared with the adult group, in the aortas of 18-month-old rats the protein expression of endothelial NO synthase (eNOS) is lower; the activity of SOD is lower but the amount of MDA is higher; the amounts of NO and cGMP are lower, but after DHEA intervention these changes are apparently ameliorated in the aged group.

CONCLUSION

During the aging process in rat arteries, the expression of eNOS is lowered, the function of oxidation resistance is weakened, and the response of the vascular smooth muscle to NO is apparently decreased. DHEA is able to ameliorate the function of NO-related signal pathways and delay the aging process of the blood vessels.

摘要

背景

衰老,尤其是血管衰老,是心脑血管疾病发生和发展中的一个危险独立因素。然而,血管衰老背后的细胞和分子病理机制仍不清楚。

目的

观察衰老过程中动脉内一氧化氮(NO)途径的变化以及脱氢表雄酮(DHEA)的干预作用。

方法

将雄性Wistar大鼠分为3个实验组,每组6只:第1组,成年对照,12月龄大鼠喂常规饲料;第2组,18月龄大鼠喂常规饲料;第3组,12月龄时在基础饲料中给予1mg/kg DHEA的18月龄大鼠。选取胸主动脉。采用蛋白质印迹法测定内皮型一氧化氮合酶蛋白,采用Griess法测定NO含量,采用放射免疫分析法测定cGMP含量,采用比色法测定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。

结果

与成年组相比,18月龄大鼠主动脉中内皮型一氧化氮合酶(eNOS)的蛋白表达较低;SOD活性较低但MDA含量较高;NO和cGMP含量较低,但经DHEA干预后,老年组的这些变化明显改善。

结论

在大鼠动脉衰老过程中,eNOS表达降低,抗氧化功能减弱,血管平滑肌对NO的反应明显降低。DHEA能够改善NO相关信号通路的功能,延缓血管衰老进程。

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