The Protective Mechanism of Ligustrazine Against Renal Ischemia/Reperfusion Injury

BackgroundIschemia/reperfusion (I/R) injury is unavoidable in renal transplantation, and represents an additional risk factor for the late renal allograft failure. Our study focused on the effects of ligustrazine on oxidative stress, apoptosis, neutrophils recruitment, the expression of proinflammatory mediators and adhesion molecules caused by renal I/R injury.Materials and MethodsRenal warm I/R was induced in male C57BL/6 mice by clamping the left renal artery and vein non-traumatically. Group I was sham-operated animals; group II, nontreated animals; and group III, ligustrazine-treated animals (80mg/kg, i.p. 30min before I/R). Mice were sacrificed 4 and 24h post reperfusion. The effects of ligustrazine on oxidative stress, neutrophils recruitment, proinflammatory mediators, and adhesion molecules caused by renal I/R injury were assayed.ResultsLigustrazine pretreatment attenuated dramatically the injuries in mice kidneys caused by warm I/R (histological scores of untreated versus treated, 4.2 ± 0.4 versus 0.9 ± 0.3; P < 0.01). Administration of ligustrazine significantly reduced myeloperoxidase (MPO) activity by 38.6% and decreased malondialdehye (MDA) level by 19.2%, while superoxide dismutase (SOD) activity increased by 39.6% (P < 0.01), suggesting an effective reduction of oxidative stress following ligustrazine treatment. Moreover, ligustrazine also inhibited cell apoptosis, abrogated neutrophils recruitment, and suppressed the over expression of TNF-α and ICAM-1.ConclusionsIn conclusion, ligustrazine protects murine kidney from warm ischemia/reperfusion injury, probably via reducing oxidative stress, inhibiting cell apoptosis, decreasing neutrophils infiltration, and suppressing the overexpression of TNF-α and ICAM-1 levels.