Cao Z.-P.,Second Peoples Hospital of Chaohu |
Cheng C.-S.,Second Peoples Hospital of Chaohu |
Zhao Z.-W.,Second Peoples Hospital of Chaohu |
Shan H.-M.,Second Peoples Hospital of Chaohu
Journal of Clinical Rehabilitative Tissue Engineering Research | Year: 2010
BACKGROUND: Recent studies have demonstrated that ligustrazine removed oxygen-derived free radicals and protected vascular endothelial cells. Howerver, the effect of ligustrazine on skin flap ischemia-reperfusion injury was less reported. OBJECTIVE: To investigate the effect of ligustrazine on skin flap ischemia-reperfusion injury, and to analyze reaction pathway. METHODS: A total of 24 healthy SD rats were used to establish ischemia-reperfusion injured skin flap along superficial epigastric artery. All rats were randomly divided into sham-surgery, model control, and ligustrazine groups, with 8 rats per group. Ischemia-reperfusion injury was not induced in the sham-surgery group; saline (4 mL/kg) was given in the model control gorup 30 minutes prior to operation; an intraperitoneal injection of ligustrazine (4 mL/kg) was given in the ligustrazine group immediately after ischemia-reperfusion injury. Distal tissue was selected from skin flap in the model control group immediate after formation of skin flap, 8 hours after ischemia, and 1 hour after reperfusion, as well as in the sham-surgery group immediate after formation of skin flap, 8 and 9 hours after operation to measure superoxide dismutase (SOD) and malonaldehyde (MDA) contents. Histological morphology was observed under optic and electron microscopes. RESULTS AND CONCLUSION: At 8 hours after ischemia and 1 hour after reperfusion, SOD activity in the model control group was significantly less than in the sham-surgery group (P < 0.05-0.01), but the SOD activity in the ligustrazine group was significantly greater than in the model control group (P < 0.05-0.01). At 1 hour after reperfusion, MDA content in the model control group was significantly greater than sham-surgery group (P < 0.01), but the MDA content in the ligustrazine group was significantly less than in the model control group (P < 0.01). As compared with model control group, ultramicrostructure and vascular endothelial cell were mildly damaged in the ligustrazine group, suggesting that ligustrazine inhibited activation and adhesion of neutrophilic granulocytes, relieved inflammatory reaction, protected endothelial cells, resisted lipid peroxidation of free radicals, and prevented skin flap ischemia-reperfusion injury.