Allicin protects against renal ischemia-reperfusion injury by attenuating oxidative stress and apoptosis

Background Studies have demonstrated that allicin may play critical roles in the procession of ischemia-reperfusion(I/R) injury. The purpose of this study was to investigate the protective effects of allicin on renal I/R injury by attenuating oxidative stress and apoptosis. Methods To establish a model of renal I/R, the right kidney underwent 12 h reperfusion after 45 min ischemia, allicin was administered intraperitoneally at concentrations of 40, 50 or 60 mg/kg. NRK-52E cells were treated with allicin at concentrations of 1, 3 or 5 mu M in 24 h hypoxia/ 6 h reoxygenation(H/R) treatments. Indicators of HE, oxidative stress, apoptosis were measured to evaluate the effect of aliicin on renal I/R injury. Results Allicin protected renal I/R injury by ameliorating histological injury and decreasing the oxidative stress in renal tissues. Meanwhile, allicin significantly downregulated the expression of Bax and caspase-3, upregulated the expression of Bcl-2 in I/R renal tissues and H/R treated NRK-52E cells. Conclusions Allicin may exert anti-apoptotic and antioxidative effects to promote renal function recovery in I/R renal tissues and H/R treated NRK-52E cells. Taken together, allicin may be a potential novel therapy option for future renal injury protection.

Automated summary

The study demonstrated that allicin protects against renal ischemia-reperfusion injury by ameliorating histological damage and reducing oxidative stress in renal tissues. Additionally, allicin was found to regulate the expression of apoptosis-related proteins in both I/R renal tissues and H/R treated NRK-52E cells, suggesting its potential as a novel therapy option for renal injury protection.