关键词: 间苯三酚, 肾, 再灌注损伤, 氧化性应激, 细胞凋亡

Abstract:

Objective：To investigate the effect and mechanisms of Phloroglucinol (PG) on renal ischemia and reperfusion injury (IRI). Methods: Forty-eight male Wistar rats were divided into 3 groups (16 rats per group): sham operated, saline-treated I/R （I/R）, and PG-treated I/R (PG). I/R model: After removing the right kidney, renal I/R injury was induced by clamping the left renal artery for 45 min followed by reperfusion. The rats were administered with PG (30 mg/kg, intraperitoneally) or saline 15 min before renal ischemia. The blood and kidneys were harvested 6 and 24 h after reperfusion. Renal function and histologic changes of serum creatinine (SCr) and blood urea nitrogen(BUN)were assessed. Malondialdehyde (MDA),catalase (CAT）,superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px）were measured. Nuclear factor-kapa B (NF-κB) and caspase-3 in the kidneys were also measured. Results: SCr and BUN were (103.9±10.4) μmol/L and (15.2±1.0) mmol/L in I/R group, and (81.8±13.4) μmol/L and (11.5±1.2) mmol/L in PG group 6 h after reperfusion. SCr and BUN were (154.9±12.1) μmol/L and (28.1±1.4) mmol/L in I/R group, and (103.8±5.9) μmol/L和(16.0±1.0) mmol/L in PG group 24 h after reperfusion.PG treatment significantly attenuated renal dysfunction and histologic damage caused by I/R injury（P<0.05）.The I/Rinduced elevation in kidney MDA level decreased, where as reduced kidney SOD,CAT and GSH-Px were increased. What is more, the apoptotic tubular cells, the levels of active caspase-3,and active nuclear factor kappa B dramatically decreased after PG treatment. Conclusion: PG protects murine kidney I/R injury by suppres-sing oxidative stress, inflammation, and cell apoptosis.

Key words: Phloroglucinol, Kidney, Reperfusion injury, Oxidative stress, Apoptosis