Significance of intervention with lipoxin A4 in rats with juvenile metabolic syndrome

Abstract

Objective To explore the protective role of lipoxin A4 (LXA4) during early process of atherosclerosis formation in rats with juvenile metabolic syndrome (MS). Methods Rat models of juvenile MS were established with 3-week Sprague-Dawley (SD) rats fed on high-carbonhydrates and high-fat diet for 6 weeks.The other quali-fied ones were randomly grouped into model group, LXA4 low-dose group, LXA4 middle-dose group, and LXA4 high-dose group, and a control group fed with normal forage.The low, middle, high-dose groups were injected different doses of LXA4 daily, while the model group and control group were injected with the same dose of isotonic NaCl solution for 2 consecutive weeks.After 2-week medication, the visceral adipose tissue were isolated by laparotomy and heart blood collected by thoracotomy under anesthesia, followed the fixation of thoracic and abdominal aortas in the immobilized rats.The mRNA expression level of inflammation cytokines interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) in the adipose tissue were determined by semi-quantitative reverse transcription PCR (RT-PCR), respectively.Secretions of IL-6, and TNF-α in serum were determined by enzyme linked immunosorbent assay (ELISA). Immunocytochemistry was used to label endomembrane and middle-membrane of thoracic aorta, and endothelial cell layer in each group and the ratios of thickness of endomembrane and middle-membrane were compared. Results Compared with the control group, weight, body length and abdominal circumference of juvenile MS rats increased significantly (all P 0.05). Compared with control group, inflammatory cytokines IL-6, TNF-α secreted in serum of model rats were increased significantly (all P 0.05). Conclusions The increasing inflammatory cytokines are involved in early process of atherosclerosis formation in rats with juvenile MS.LXA4 by reducing the expression of inflammatory factor level in adipose tissue, thereby reducing the inflammatory cytokines in serum, alleviate the damage of arterial wall. Key words: Metabolic syndrome; Lipoxin A4; Inflammatory cytokine; Interleukin-6; Tumor necrosis factor-α; C-reactive protein; Atherosclerosis