The protective effects of propofol against renal ischemia-reperfusion injury are potentiated by norisoboldine treatment via inhibition of oxidative stress pathways

Acute kidney injury (AKI) is a significant worldwide health problem. The protective effects of norisoboldine (NOR) against ischemia/reperfusion (I/R) induced renal injury in a rat model were evaluated. AKI was induced in rats by I/R. Animals were treated with 20 mg/kg/h propofol, intraperitoneally administered and 10 mg/kg NOR 30 min before inducing renal ischemia. Biomarkers of kidney function, including cytokines and oxidative stress parameters, were measured in serum. The serum levels of creatinine and blood urea nitrogen in propofol- and NOR-treated rats were lower compared to the untreated I/R group. Moreover, treatment with propofol or NOR, alone and in combination, decreased the levels of cytokines and oxidative stress in rats with kidney injury. In conclusion, this study suggested that treatment with NOR potentiated the nephroprotective effects of propofol in rats with I/R-induced renal injury by ameliorating oxidative stress and apoptosis pathway.

Automated summary

This study demonstrated that NOR has protective effects against I/R-induced renal injury, enhancing the nephroprotective effects of propofol, and reducing levels of creatinine and blood urea nitrogen. Treatment with propofol or NOR, alone and in combination, also decreased cytokine and oxidative stress levels in rats with kidney injury.