Protective effects of interleukin‐2 against endothelial dysfunction induced by high glucose

The objective of the present study was to explore whether interleukin‐2 (IL‐2) has protective effects against endothelial dysfunction induced by high glucose via the nitric oxide (NO) mechanism. Acetylcholine‐induced endothelium‐dependent relaxation (EDR), sodium nitroprusside‐induced endothelium‐independent relaxation (EIR) and biochemical parameters including superoxide dismutase (SOD) and nitric oxide synthase (NOS) were measured in non‐diabetic rat isolated aorta in condition of high glucose concentration. EDR, EIR and serum NO levels in streptozotocin‐induced diabetic rats were also measured. A 4 h incubation of aortic rings with high glucose (44 mmol/L) resulted in a significant inhibition of EDR, but had no effects on EIR. Co‐presence of IL‐2 (100 and 1000 U/ml) for 40 min prevented the inhibition of EDR caused by high glucose. However, this effect of IL‐2 was canceled by pretreatment with L‐NAME. Similarly, high glucose decreased SOD and NOS activities in aortic tissues. IL‐2 (1000 U/ml) significantly attenuated the decrease of SOD and NOS activities caused by high glucose in aortic tissues. Mannitol (44 mmol/L) alone had no effect on EDR, EIR and biochemical parameters. In addition, EDR, but not EIR was declined in company with the decrease of serum NO level in diabetic rats. Injection of IL‐2 (5000 and 50000 U/kg/d, s.c.) for 5 weeks prevented the decrease of EDR and serum NO level in diabetic rats. The results indicate that IL‐2 prevents endothelial dysfunction induced by high glucose or hyperglycemia via, at least partly, activation of NOS and SOD.