Irbesartan inhibits high glucose-induced lipid oxidation effect and human umbilical vein endothelial cell injury

Objective: To discuss the influences of irbesartan on high glucose-induced lipid oxidation effect and human umbilical vein endothelial cell (HUVEC) injury. Methods: HUVECs of the logarithmic phase were divided into four groups: normal-concentration glucose control group (glucose final concentration of 5.5 mmol/L), high-glucose group (glucose final concentration of 33.3 mmol/L), irbesartan intervention group, and anti-oxidant N-acetyl-cysteinyl acid (NAC) intervention group. The intervention groups were first treated with irbesartan (10^-5 mmol/L) and NAC (10 mmol/L) for 1 h, respectively, then co-incubated with high glucose (glucose final concentration of 33.3 mmol/L) for 24 h, 48 h and 72 h. Malondialdehyde (MDA) content and superoxide dismutase (SOD) activity of culture supernatant were determined by TBARS method and spectrophotometric assay, respectively. Results: MDA content increased significantly (P<0.01) and SOD activity decreased significantly (P<0.01) in high glucose group compared with control group. MDA content reached a considerable level (P<0.05) when HUVECs were treated with high glucose for 24 hours; with time prolonging for 48 hours and 72 hours, the level of MDA had a slightly upward trend, but with no statistical significance (P>0.05). Compared with that in high glucose group, MDA content significantly decreased (P<0.05) and SOD activity significantly increased (P<0.05) in irbesartan- and NAC-treated groups. Apoptosis of HUVECs was significantly reduced (both P<0.05) at each time point in irbesartan- and NAC-treated groups, and the damage of high glucose on morphology of HUVECs also reduced significantly. Conclusion: Irbesartan reduces lipid oxidation induced by high glucose partially by inhibiting oxidative stress and thus protects HUVEC.