Isoquercitrin Attenuates Renal Ischemia/Reperfusion Injury Through Antioxidation, Anti-inflammation, and Antiapoptosis in Mice.

Renal ischemia-reperfusion injury (RIRI) occurs after several surgical procedures such as kidney transplantation and partial nephrectomy. Isoquercitrin (IQ) exhibited protective effects in cerebral ischemia-reperfusion injury. In the present study, we aimed to evaluate the effects of IQ on the prevention of RIRI. The mouse model of RIRI was induced by 30-minute clamping of the left renal pedicle after excising of the right kidney, followed by 24-hour reperfusion. Thirty mice were randomly divided into the following 3 groups: sham operation, RIRI model group, and IQ pretreatment + RIRI. Serum creatinine and blood urea nitrogen (BUN) were used for evaluating renal function. Kidney cell apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Moreover, the pro-inflammatory cytokines (TNF-α, IL-6), the oxidative stress associated factors (malondialdehyde, superoxide dismutase), and the apoptotic factors (Bcl-2, Bax) were assessed. After RIRI, BUN, creatinine, TNF-α, IL-6, malondialdehyde, and Bax were significantly increased, and levels of superoxide dismutase and Bcl-2/Bax ratio and Bcl-2 expression were decreased markedly. As expect, IQ reversed these changes. These data indicate that IQ plays a protective role during RIRI, which may be partially mediated through the actions of antioxidation, anti-inflammation, and antiapoptosis. • This is the first study, to our knowledge, to demonstrate the renoprotective effect of isoquercitrin against renal ischemia/reperfusion injury in a mouse model. • Isoquercitrin protects against renal ischemia/reperfusion injury by alleviating inflammatory responses, reducing oxidative stress, and attenuating apoptosis. • The mechanism of isoquercitrin inhibiting apoptosis-induced renal ischemia-reperfusion injury was mediated by up-regulation of the ratio of Bcl-2/Bax. [ABSTRACT FROM AUTHOR]