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

Abstract

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 μM 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.

Keywords: Allicin; Apoptosis; Reactive Oxygen Species; Renal ischemia–reperfusion injury.

Fig. 1

Allicin alleviates histopathological damage and reduces levels of oxidative stress after renal I/R in rats. A Hematoxylin and eosin (H&E, × 200) staining was measured to evaluate renal tubule injury in renal tissues. B MDA content and SOD activity were measured to evaluate the level of oxidative stress. (A) control group, (B) sham group, (C) I/R group, (D) I/R + 40 mg/kg allicin group, (E) I/R + 50 mg/kg allicin group and (F) I/R + 60 mg/kg allicin group. *p < 0.05 vs. group A and B; ^#p < 0.05 vs. group C

Fig. 2

Allicin inhibits the apoptosis of renal tubular epithelial cells after renal I/R in rats. A Apoptosis index (AI) in the 6 groups (magnification, × 200). B Immunohistochemistry was performed to measure the expression of Bax, caspase-3 and Bcl-2 (magnification, × 200). C The protein expression of Bax, cleaved caspase-3 and Bcl-2 was detected by western blot. GAPDH was as a loading control. (A) control group, (B) sham group, (C) I/R group, (D) I/R + 40 mg/kg allicin group, (E) I/R + 50 mg/kg allicin group and (F) I/R + 60 mg/kg allicin group. *p < 0.05 vs. group A and B; ^#p < 0.05 vs. group C

Fig. 3

Allicin inhibits the apoptosis of renal tubular epithelial cells induced by H/R in NRK-52E cells. A Cell apoptosis of NRK-52E cells was examined by flow cytometry. B The protein expression of Bax, cleaved caspase-3 and Bcl-2 was detected by western blot. GAPDH was as a loading control. C The mRNA expression of Bax, caspase-3 and Bcl-2 was evaluated by qRT-PCR analysis. (A) control group, (B) H/R group, (C) H/R group + 1 μM allicin group, (D) H/R + 3 μM allicin group, (E) H/R + 5 μM allicin group. *p < 0.05 vs. group A; ^#p < 0.05 vs. group B