RESUMO
Food deprivation protects against ischemia-reperfusion (IR) injury through unknown mechanisms. In an experimental rat model of acute IR injury, we found that preoperative fasting for 3 days protects rats from tubular damage and renal functional decline by increasing antioxidant protection independently of the NF-E2-related factor 2 (Nrf2), and by maintaining mitochondrial morphology and function. In addition, further analysis revealed that fasting protects against tubulointerstitial fibrosis. In summary, our results point out to fasting as a robust nutritional intervention to limit oxidative stress and mitochondrial dysfunction in early acute kidney injury and also to promote long-term protection against fibrosis.
Assuntos
Injúria Renal Aguda/dietoterapia , Rim/metabolismo , Fator 2 Relacionado a NF-E2/genética , Traumatismo por Reperfusão/dietoterapia , Injúria Renal Aguda/genética , Injúria Renal Aguda/metabolismo , Injúria Renal Aguda/patologia , Animais , Antioxidantes/metabolismo , Jejum/metabolismo , Fibrose/dietoterapia , Fibrose/metabolismo , Fibrose/patologia , Privação de Alimentos , Humanos , Rim/lesões , Rim/patologia , Túbulos Renais/metabolismo , Túbulos Renais/patologia , Malondialdeído/metabolismo , Mitocôndrias/metabolismo , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/genética , Ratos , Traumatismo por Reperfusão/genética , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologiaRESUMO
In this paper, we review recent evidence about the beneficial effects of sulforaphane (SFN), which is the most studied member of isothiocyanates, on both in vivo and in vitro models of different diseases, mainly diabetes and cancer. The role of SFN on oxidative stress, inflammation, and metabolism is discussed, with emphasis on those nuclear factor E2-related factor 2 (Nrf2) pathway-mediated mechanisms. In the case of the anti-inflammatory effects of SFN, the point of convergence seems to be the downregulation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), with the consequent amelioration of other pathogenic processes such as hypertrophy and fibrosis. We emphasized that SFN shows opposite effects in normal and cancer cells at many levels; for instance, while in normal cells it has protective actions, in cancer cells it blocks the induction of factors related to the malignity of tumors, diminishes their development, and induces cell death. SFN is able to promote apoptosis in cancer cells by many mechanisms, the production of reactive oxygen species being one of the most relevant ones. Given its properties, SFN could be considered as a phytochemical at the forefront of natural medicine.