The influence of trimetazidine hydrochloride on acute ischemia-reperfusion injury of endothelial cells and oxidative stress response of rat kidney

Objective To observe the effects of trimetazidine (TMZ) preconditioning on endothelial cell injury and oxidative stress in rats with acute renal ischemia-reperfusion. Methods 90 SD rats were randomly divided into A and B groups. Group A was given TMZ at a dose of 10 mg/kg. After lavaged for 5 days, ischemia-reperfusion injury (IR1), ischemic postconditioning (IPO1), sham operated (S1) were established. In the same way, the IR2, IPO2 and S2 were established in group B after 5 days of saline enema. The levels of serum creatinine (SCr), urea nitrogen (BUN), vascular cell adhesion molecule 1 (VCAM-1), malondialdehyde (MDA) superoxide dismutase (SOD) were measured at 0, 6, 12, 24 and 48 h after the last recovery of kidney blood supply in each group. Results Compared with IR1 group, the levels of VCAM-1, MDA at 6 h and BUN, SCr, VCAM-1, MDA and renal tubular injury score at 24 and 48 h in IR2 group were significantly higher than those in IR1 group, while SOD was decreased; Compared with IPO1 group, the levels of VCAM-1 and MDA at 6, 12 and 24 h and BUN, SCr and renal tubular injury score at 24 h in IPO2 group were significantly increased, while SOD was decreased at 6, 12 and 24 h; Compared with IPO1, apart from SCr, the levels of BUN, VCAM-1, MDA and renal tubular injury score at 24 h in IR1 group were increased and the levels of VCAM-1, renal tubular injury score at 48 h in IR1 group were significantly increased, and SOD was decreased at both time points; Compared with IR1 group, the levels of VCAM-1, MDA and renal tubular injury score at 12 and 24 h in IPO2 group were increased, while SOD were decreased and apart from MDA, the levels of BUN, SCr, VCAM-1 and renal tubular injury score at 48 h in IPO2 group were significantly increased, while SOD was decreased (P>0.05). Conclusions Compared with IPO alone, using TMZ can reduce the oxidative stress response and decrease the serum VCAM-1 level before the occurrence of IR in rats.