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内源性睾丸酮可增加自发性高血压大鼠的白细胞-内皮细胞相互作用。

Endogenous testosterone increases leukocyte-endothelial cell interaction in spontaneously hypertensive rats.

机构信息

Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.

出版信息

Life Sci. 2012 May 15;90(17-18):689-94. doi: 10.1016/j.lfs.2012.03.009. Epub 2012 Apr 1.

Abstract

AIMS

Inflammation may have an important role in the beginning and in the progress of cardiovascular diseases. Testosterone exerts important effects on vascular function, which is altered in arterial hypertension. Thus, the aim of this study was to evaluate the influence of endogenous testosterone on leukocyte behavior in post-capillary venules of the mesenteric bed of spontaneously hypertensive rats (SHR).

MAIN METHODS

18 week-old intact SHR, castrated SHR and normotensive rats (intact Wistar) were used. Blood pressure was measured by tail plethysmography and serum testosterone levels by ELISA. Leukocyte rolling, adhesion and migration were evaluated in vivo in situ by intravital microscopy.

KEY FINDINGS

Castration significantly reduced blood pressure and reversed the increased leukocyte rolling and adhesion observed in SHRs. Leukocyte counts and other hemodynamic parameters did not differ among groups. SHRs displayed increased protein expression of P-selectin and ICAM-1 in mesenteric venules when compared to intact Wistar. Castration of SHRs restored the protein expression of the cell adhesion molecules.

SIGNIFICANCE

The findings of the present study demonstrate the critical role of endogenous testosterone mediating the effects of hypertension increasing leukocyte-endothelial cell interaction. Increased expression of cell adhesion molecules contribute to the effects of endogenous testosterone promoting increased leukocyte rolling and adhesion in SHRs.

摘要

目的

炎症可能在心血管疾病的发生和发展中起重要作用。睾酮对血管功能有重要影响,而动脉高血压会改变血管功能。因此,本研究旨在评估内源性睾酮对自发性高血压大鼠(SHR)肠系膜床后毛细静脉中白细胞行为的影响。

主要方法

使用 18 周龄完整 SHR、去势 SHR 和正常血压大鼠(完整 Wistar)。通过尾容积描记法测量血压,通过 ELISA 测量血清睾酮水平。通过活体显微镜评估体内白细胞滚动、黏附和迁移。

主要发现

去势显著降低了血压,并逆转了 SHR 中观察到的白细胞滚动和黏附增加。白细胞计数和其他血流动力学参数在各组之间没有差异。与完整 Wistar 相比,SHR 的肠系膜静脉中 P-选择素和 ICAM-1 的蛋白表达增加。SHR 的去势恢复了细胞黏附分子的蛋白表达。

意义

本研究的结果表明,内源性睾酮介导高血压增加白细胞-内皮细胞相互作用的作用至关重要。细胞黏附分子的表达增加有助于内源性睾酮促进 SHR 中白细胞滚动和黏附的作用。

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