Effects of antioxidant on the gene expression of ?_1-adrenergic receptors during endotoxic shock in rats / 中华麻醉学杂志

ABSTRACT

Objective To investigate the effects of antioxidant on the gene expression of ?1-adrenergic receptors (AR) during endotoxic shock. Methods Forty male SD rats weighing 200-250 g were anesthetized with intraperitoneal (i.p.) pentobarbital. The animals kept spontaneous breathing. Femoral artery and vein were cannulated for BP monitoring and drug administration. The animals were randomly divided into 5 groups ( n = 8 each) (1) control group; (2) LPS group received IPS 15 mg?kg-1 i.v. ; (3) LPS + propofol group received at 1h after LPS a bolus of propofol 10mg?kg-1 i.v. followed by continuous infusion of propofol at 10 mg?kg-1?h-1; (4) LPS + uric acid (UA) group received uric acid 200 mg i.p. 1 h after LPS and (5) LPS + melatonin (MLT) group received MLT 10 mg?kg-1 i.p. 1h after LPS. The animals were killed at 6 h after LPS. Total RNA was extracted from the heart, aorta, vein, lung, liver and kidney. ?1A-,?1B-,?1D- AR mRNA and ?-actin mRNA were measured using reverse transcription polymerase chain reaction (RT-PCR) .Results The expression of ?1A-AR and ?1B-AR mRNA in all the organs and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were strongly down-regulated in LPS group. In group 3 (LPS + propofol) the expression of ?1A-AR mRNA in the lung and kidney, the ?1B-AR mRNA expression in all of the organs and ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly increased as compared with LPS group. There was no significant difference in ?1-AR mRNA expression between LPS group and LPS + MLT group. The expression of ?1A-AR mRNA in kidney, the ?1B-AR mRNA expression in all of the organs except the lung and the ?1D-AR mRNA expression in aorta, liver, lung and kidney were significantly higher in LPS + UA group than in LPS group. Conclusion Circulatory failure induced by endotoxic shock is related to the down-regulation of ?1-AR gene expression. The therapeutic effects of antioxidant on the endotoxic shock is partly due to up-regulation of ?1-AR gene expression.