Goto-Kakizaki rats developing type 2 diabetes mellitus were randomly assigned to one of the following groups: sham (n = 10), CPB (CPB alone, n = 9), or EGCG (CPB + EGCG, n = 10). CPB was conducted for 30 minutes at a flow rate of 100 mL/kg/min in the CPB and EGCG groups. Rats assigned to the EGCG group were administrated EGCG solution orally for 2 weeks before CPB. We evaluated renal biochemical or histologic changes at 24 hours after CPB.
Compared with the CPB group, the EGCG group exhibited milder tubular injury histologically (p < 0.0001) and reduced expression of kidney injury molecule-1, a biomarker for renal tubular injury (p < 0.0001) and 8-hydroxy-2′-deoxyguanosine (p < 0.01), indicating attenuated oxidant stress.
Preoperative oral administration of EGCG ameliorates AKI in a CPB model of diabetic rats through antioxidative properties. This simple method could be applied in a clinical setting as a prophylactic renal protection against AKI after CPB, especially for high-risk patients with diabetes mellitus.