Abstract

Male WKY and SHR rats were separated into five groups: Control, FFR: WKY rats receiving a 10% (w/v) fructose solution during all 12 weeks, SHR, FFHR: SHR receiving a 10% (w/v) fructose solution during all 12 weeks and FFHR+Mtx (0,3 mg/kg intraperitoneal one injection per day week for 6 weeks) (n = 8 per group). Metabolic variables and systolic blood pressure were measured. Cardiac and vascular remodelling was also evaluated. To assess this, IL-6R and VCAM-1 immunostaining techniques were used.

Highlights

  • Increasing evidence suggests that immune activation and inflammatory mediators may play a role in the development and progression of atherosclerosis

  • The comparison between the HOMA index and the areas under the glucose tolerance test (GTT) curve indicated that the Fructose-fed rats (FFR) and Fructose-fed hypertensive rats (FFHR) developed glucose intolerance, as demonstrated by the significantly increased HOMA index and area values compared to the control rats (Table 1)

  • The animals in the FFR and FFHR groups displayed significant differences in the levels of triglycerides and HDL-cholesterol when compared to the controls (Table 1)

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Summary

Introduction

Increasing evidence suggests that immune activation and inflammatory mediators may play a role in the development and progression of atherosclerosis. Several studies have shown that patients with some diseases characterized by inflammatory mediator activation, which rheumatoid arthritis (RA), presented accelerate atherosclerosis. The age- and sex-adjusted mortality rate for cardiovascular disease (CVD) in RA patients is 50%-100% higher than the rate in the general population [4]. The traditional atherosclerotic risk factors alone cannot explain the accelerated atherosclerosis in RA patients. Some studies have reported that chronic inflammation might play a major role in accelerated atherosclerosis [6]. We used Methotrexate (Mtx) to examine the role of immunomodulation on the activation of IL-6 and VCAM-1, which could generate a microenvironment that supports cardiovascular remodelling

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