Inhibitory effects of adrenomedulin on expression of vascular cell adhesion molecule-1 in rats with myocardial ischemia-reperfusion injury

Yuting BAI; Qing MIN; Jingzhi WAN; Hui GAO

ABSTRACT

BACKGROUND:

Calcitonin gene-related peptide(CGRP) can relieve myocardial ischemia-reperfusion injury. Because adrenomedulin(Adm) and CGRP share certain structural homology, it is assumed that Adm might have protective effect on myocardium.

OBJECTIVE:

To investigate Adm' s inhibitory effect on vascular cell adhesion molecule-1 (VCAM-1) expression in ischemia-reperfusion rats and its protective effect on myocardial ischemia.

DESIGN:

A randomized paired design using ischemia-reperfusion model of SD rats.MATERIALS The experiment was conducted in the Experimental Animal Center of Xianning Medical College from December 2003 to May 2004. Twenty-four healthy male SD rats were selected.

METHODS:

The hearts of the rats were removed to make into ischemia-reperfusion model and then randomized to control group, Adm1-50(1× 10-9) mol/L group, Adm1-50(1 × 10-8) mol/L group and Adm1-50(1 × 10-7) mol/L group. After the hearts underwent ischemia for 60 minutes, the hearts in control group were reperfused with oxygenation Kerbs-Henseleit bicarbonate(KHB) for 60 minutes while those in the other three groups had reperfusion with oxygenation KHB and Adm1-50( 1 × 10-9),(1 × 10-8), and(1 × 10-7) mol/L, respectively, for 15 minutes and KHB perfusion for another 45 minutes. The liquid flowing from the coronary artery was collected, and the content of creatine kinase isoenzyme was detected. Myocardium in the left ventricle was collected for RNA extraction, and the expression of VCAM-1m RNA was determined with reverse transcription-polymerase chain reaction method.MAIN OUTCOME

MEASURES:

The expression of myocardial VCAM-1mRNA in control group and groups of different concentrations of Adm1-50.

RESULTS:

After electrophoresis, each group was found to have an obvious amplified band at 194bp, which was GADPH mRNA amplified segment, and the expression of GADPH mRNA in each group was the same. VCAM-1 mRNA amplified segment with strong brightness and clear border was found at 334bp in control group and Adml-50 (1 × 10-9) mol/L group. The brightness of VCAM-1 mRNA amplified band decreased significantly in Adm1-50(1 × 10-8) mol/L group whereas slight brightness and obscure amplified band was found in Adm1-50(1 × 10-7) mol/L group. The gray value of amplified VCAM-1mRNA and GAPDH mRNA in Adm1-50(1 × 10-8)group and(1 × 10-7) mol/L group was 0.6 ±0.31 and 0.5 ±0.36, respectively, which was obviously lower than that in control group( 1.2 ± 0. 52) ( P＜ 0. 05).

CONCLUSION:

Adm1-50 may inhibit the expression of myocardial VCAM-1mRNA in myocardial ischemia-reperfusion in a dose-dependent manner.