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Allicin has been reported to play a biological role in human pathophysiological processes via interaction with numerous signaling pathways and gene expression alteration. The purpose of the present study was to evaluate the protective effects of allicin against renal ischemia/reperfusion injury (RIRI) in rats. In the present study, the RIRI model with 45-min ischemia and 22-h reperfusion in rats was generated and allicin was used as the intervention. Changes in renal tissue pathomorphology, renal function, oxidative stress, inflammatory response and apoptosis were evaluated in the RIRI model in rats. Compared with those in the RIRI group, renal function, renal pathological injury, and anti-inflammatory and antioxidant properties were markedly improved in the RIRI+allicin group. Thus, our research suggested that allicin exerted its protective effect against ischemia/reperfusion-induced renal injury by regulating apoptosis, oxidative stress and inflammatory response in rats. [Display omitted] • Pretreatment with allicin could regulate renal function impairment induced by ischemia reperfusion. • Preconditioning with allicin participated in oxidative stress of RIRI. • Allicin played a vital role in RIRI by exerting anti-apoptotic and anti-inflammatory activities. [ABSTRACT FROM AUTHOR]

The main cause of chronic renal allograft dysfunction (CRAD) still remains unclear. Insulin resistance (IR) may be a potential inducement, but there is insufficient evidence about this association. We aimed to establish a rat model of CRAD complicated with IR and to explore the function and pathologic changes of the renal allograft induced by IR. F344-to-Lewis rats of CRAD were fed a high-fat diet to induce IR. They were divided into 3 groups: IR (CRAD+IR), CRAD, and control (CTL). Serum levels of blood urea nitrogen (BUN) and serum creatinine (Scr) were measured to evaluate the renal function. The Homeostasis Model Assessment (HOMA)-IR index was detected by comparing the values of fasting serum insulin levels (FINS) with fasting blood glucose levels (FBG). The pathologic analysis was conducted by the degree of renal lesions including glomerular lesions, renal tubular lesions, hemorrhage, inflammatory cell infiltration, fibrillation, and hyperplasia of the renal interstitium. In the second, third, and fourth month after surgery, serum levels of Scr and BUN in the IR group were reduced more than those in the CRAD group, while they were both higher compared to the CTL group, suggesting that renal function in the CRAD group was declined. The HOMA-IR in the IR group was greater than that in the CRAD and CTL groups, showing that simple high-fat diet feeding significantly and steadily increased FINS and FBG in CRAD complicated with IR rats. Pathologic changes indicated that the CRAD rat model was successfully constructed and was still in the early-middle stages of renal lesions 4 months after surgery, yet IR presented a significant effect on CRAD. These results indicate that the stable CRAD complicated with IR rat model can be established through a high-fat diet in CRAD rats in 4 months, and IR could be an influencing factor. • Stable CRAD complicated with IR rat models can be established via a high-fat diet, in which IR could be an influencing factor. • Simple high-fat diet feeding steadily increased FINS and FBG in rats with CRAD complicated with IR. • HOMA-IR in the IR group was greater than that in the CRAD and CTL groups. [ABSTRACT FROM AUTHOR]