[Effect of aerobic interval training on the expression of renal CD40 in a rat model with myocardial infarction and its mechanism].

OBJECTIVE

To study the effects of aerobic interval training (AIT) on renal cluster of differentiation 40 (CD40) expression in rats with myocardial infarction (MI) and its possible mechanism.

METHODS

Thirty-six rats were randomly divided into three groups (=12):Sham, MI and MI with AIT (ME) groups. The MI model was established by ligation of the left anterior descending coronary artery. Treadmill training was performed five times a week for 8 weeks (AIT:60 min/day with 10 min of warm-up at 10 m/min and 50 min of exercise at 25 m/min 7 min interspersed with 3 min at 15 m/min). After training, cardiaorenal function and renal tissue remodeling were evaluated. The changes of CD40, high-sensitivity C reactive protein(hs-CRP), TNF-α, IL-6, p-NF-κBp65, blood urea nitrogen (BUN) and serum creatinine (sCr) were determined.

RESULTS

Compared with the sham group, MI significantly increased left ventricular end-diastolic pressure (LVEDP) and decreased left ventricular systolic pressure (LVSP) and left indoor pressure change rate peak (dp/dtmax) in the MI group, concomitant with the increase in renal collagen volume fraction (CVF), which was reversed by AIT in the ME group. Moreover, compared with the sham group, CD40 was largely dispersed within the cytoplasm of renal tubule cells in the MI group. Meanwhile, the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6, the phosphorylation of NF-κBp65 (p-NF-κBp65) and the levels of sCr and BUN were obviously increased in the MI group. Compared with the MI group, AIT decreased the expressions of renal CD40 mRNA and protein, the levels of serum and renal hs-CRP, TNF-α and IL-6 and the expression of p-NF-κBp65, as well as decreased the levels of sCr and BUN in the ME group.

CONCLUSIONS

AIT reduces the expressions of renal CD40 protein and mRNA, inhibits NF-κB signaling pathway, and then decreases the levels of inflammatory factors thereby improve the renal dysfunction after MI.