Propofol attenuates renal ischemia-reperfusion injury aggravated by hyperglycemia

Abstract

Hyperglycemia exacerbates renal ischemia/reperfusion injury via aggravated inflammatory response and excessive production of reactive oxygen species. This study aimed to investigate the ability of propofol, a known antioxidant, to protect kidneys against ischemia/reperfusion injury in hyperglycemic rats in comparison with normoglycemic rats. Sixty rats were randomly assigned to four groups: normoglycemia-etomidate, normoglycemia-propofol, hyperglycemia-etomidate, and hyperglycemia-propofol. Anesthesia was provided with propofol or etomidate depending on the group. Also, the rats received 1.2 g•kg–1 dextrose or the same volume of normal saline depending on the group. Renal ischemia was induced for 25 min. The rats were sacrificed and samples were collected at 65 min after starting IV anesthetics (sham) and at 15 min and 24 h after reperfusion injury to compare the histological degree of renal tubular damage, and levels of inflammatory markers and enzymes related to reactive oxygen species.Compared to etomidate, propofol significantly attenuated tubular damage after reperfusion in hyperglycemic rats. Also, tubular damage was greater under hyperglycemia compared to normoglycemia in the etomidate group whereas it was similar in the propofol group. Propofol preserved superoxide dismutase level and attenuated the increase in levels of myeloperoxidase, interlukin-1, and tumor necrosis factor-α after reperfusion compared to etomidate especially in hyperglycemic rats. Propofol also attenuated production of inducible nitric oxide synthase and phosphorylation of inhibitor of κB and nuclear factor-κB after reperfusion, which were more prominent under hyperglycemia. Propofol anesthesia conveyed reno-protection against ischemia/reperfusion injury by preserved antioxidation ability and attenuated inflammatory response, which were more prominent under hyperglycemic condition.