Effect of polydatin on inflammatory response and oxidative stress in rats with sepsis-induced acute kidney injury / 临床麻醉学杂志

ABSTRACT

Objective To determine if polydatin inhibited oxidative stress and inflammatory response in rats with sepsis-induced acute kidney injury (AKI).Methods Seventy-two rats (weighing 180-220 g) were randomly divided into the following groups sham group, cecal ligation and puncture (CLP) CLP+normal saline group (group CN), group CLP+vehicle (group CV), and group CLP+polydatin (group CD) (n=18 each).Rats in groups CN, CV and CD underwent CLP to mimic sepsis-induced AKI.In sham group, the cecum was not ligated or punched, and the remaining procedures were the same as in group CLP.Normal saline, vehicle, and 30 mg/kg polydatin were administered at 6, 12, and 18 hours after CLP via the tail vein.At 24 hour post CLP, two clinically used markers of AKI, blood urea nitrogen (BUN), and creatinine (Cr) were tested, pathological changes of kidney tissue was observed under light microscopy in each group.Renal tubular damage assessment was carried out.Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) content of renal tissue, serum cytokines such as TNF-α, IL-1β and IL-6, were also measured in each group at 24 hours after CLP.Results Compared with sham group, multiple indexes such as BUN, Cr, tubular injury scores, MDA content of renal tissue, and serum cytokines incluing TNF-α, IL-1β and IL-6 increased significantly (P<0.01), while SOD and GSH levels of renal tissue significantly decreased in groups CN and CV (P<0.01).Compared with groups CN and CV, the indicators such as BUN, Cr, tubular injury scores, MDA content of renal tissue, and serum cytokines such as IL-1β and IL-6 significantly decreased (P<0.05);while SOD and GSH levels of renal tissue significantly increased (P<0.05).Conclusion Sepsis caused by sepsis cecal ligation and puncture can cause acute kidney injury.Polydatin could alleviate kidney damage by attenuating systemic inflammatory response and inhibiting oxidative stress of renal tissue.