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cope Conjugated linoleic acids (CLAs) are dietary components with beneficial effects on human health. The aim of this study was to evaluate the potential benefits of CLA pretreatment in a rat model of renal ischemia/reperfusion injury (IRI). Methods and results Animals were treated with CLAs (200 mg/kg/day) or water for two weeks prior to sham surgery or to surgery to induce IRI. Renal function, oxidative stress, apoptosis, and cell proliferation markers, were evaluated. Moreover, kidney sections were submitted to histological evaluation. IRI induced increased serum creatinine, blood urea nitrogen, fractional sodium excretion, malondialdehyde, Bax, and phosphorylated mammalian target of rapamycin (P-mTOR), and decreased clearance of creatine, superoxide dismutase and catalase activities, and Bax in comparison with control groups. CLA prefeeding restored, at least in part, the above reported markers to normal levels, increased the anti-apoptotic protein, B-cell lymphoma 2 (Bcl-2), and reduce the histological damage. Conclusion The results suggest that the decreased renal tissue damage and improved renal function and oxidative stress, in rats pretreated with CLAs before renal IRI induction, could be associated with downregulation of Bax and P-mTOR, and upregulation of Bcl-2. CLAs pretreatment resulted to protect against IRI through the regulation of signaling pathways involved in apoptosis.

Necrosis and apoptosis caused by ischaemia-reperfusion (IR) result in myocyte death and atrophy. ATP-sensitive K(+) (K(ATP) ) channels activation increases tissue tolerance of IR-injury. Thus, in the present study, we evaluated the effects of K(ATP) channel activation on skeletal muscle apoptosis after IR. Male Wistar rats were treated with 40 mg/kg, i.p., diazoxide (a K(ATP) channel opener) or 5 mg/kg, i.p., glibenclamide (a K(ATP) channel inhibitor) 30 min before the induction of 3 h ischaemia, followed by 6, 24 or 48 h reperfusion. At the end of the reperfusion period, the gastrocnemius muscle was removed for the analysis of tissue malondialdehyde content, superoxide dismutase (SOD) and catalase (CAT) activity, Bax and Bcl-2 protein expression, histological damage and the number of apoptotic nuclei. Ischaemia-reperfusion increased malondialdehyde content (P 0.01) and Bax expression (P 0.01) and induced severe histological damage, in addition to decreasing CAT and SOD activity (P 0.01 and P 0.05, respectively) and Bcl-2 expression (P 0.01). Diazoxide reversed the effects of IR on tissue damage, MDA content, SOD and CAT activity (after 6 and 24 h reperfusion; P 0.05) and Bax and Bcl-2 expression (after 24 and 48 h reperfusion; P 0.01). In contrast, glibenclamide pretreatment had no effect. The number of apoptotic nuclei in the IR and glibenclamide-pretreated groups increased significantly (P 0.001 vs Sham). In contrast, diazoxide pretreatment decreased the number of apoptotic nuclei compared with the IR group (P 0.01). The results of the present study suggest that the K(ATP) channel activator diazoxide attenuates lipid peroxidation during the first hour of reperfusion and modulates apoptotic pathways at later time points.