N-acetilcisteína e deferoxamina protegem contra insuficiência renal aguda induzida por isquemia/reperfusão em ratos

Bernardi, R; Constantino, Larissa; Machado, Roberta; Vuolo, Francieli; Budni, Patrícia; Ritter, Cristiane; Dal‐Pizzol, Felipe

doi:10.1590/s0103-507x2012000300003

Cited by 11 publications

(2 citation statements)

References 37 publications

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“…Furthermore, the ensuing reperfusion delivers more iron to the kidney, thus exacerbating oxidative stress-induced damage. In animal studies the use of iron chelators or scavengers, such as DFO, apo-transferrin, and Lcn2, has been shown to mitigate ischemia-reperfusion AKI (23,47,119). Administering the Lcn2-siderophore-iron complex was also found to alleviate ischemia-reperfusion AKI (122) and attenuate acute rejection of renal transplants (6).…”

Section: Kidney Diseasesmentioning

confidence: 99%

Lipocalin 2: An Emerging Player in Iron Homeostasis and Inflammation

2017

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Lipocalin 2 (Lcn2), an innate immune protein, has emerged as a critical iron regulatory protein during physiological and inflammatory conditions. As a bacteriostatic factor, Lcn2 obstructs the siderophore iron-acquiring strategy of bacteria and thus inhibits bacterial growth. As part of host nutritional immunity, Lcn2 facilitates systemic, cellular, and mucosal hypoferremia during inflammation, in addition to stabilizing the siderophore-bound labile iron pool. In this review, we summarize recent advances in understanding the interaction between Lcn2 and iron, and its effects in various inflammatory diseases. Lcn2 exerts mostly a protective role in infectious and inflammatory bowel diseases, whereas both beneficial and detrimental functions have been documented in neurodegenerative diseases, metabolic syndrome, renal disorders, skin disorders, and cancer. Further animal and clinical studies are necessary to unveil the multifaceted roles of Lcn2 in iron dysregulation during inflammation and to explore its therapeutic potential for treating inflammatory diseases.

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Section: Kidney Diseasesmentioning

confidence: 99%

Lipocalin 2: An Emerging Player in Iron Homeostasis and Inflammation

2017

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“…Moreover Acute Renal Failure (ARF) causing progressive loss of renal function associated with interstitial inflammation, tubular injury and increasing Tumor Necrosis Factor (TNF) (Kim et al, 2010;Sanz et al, 2010). Antioxidants are widely used in animal models to prevent acute renal failure such as the protective effects of N-acetylcysteine, N-acetylcysteine plus deferoxamine, vitamin C and vitamin E. (Bernardi et al, 2012;Kongkham et al, 2013;Aldallal, 2013). Vitamin E modulate Glutathione Peroxidase (GPx) activity in kidney, GPX play a critical role as antioxidant defense system by catalyzing detoxification of hydrogen peroxide (H 2 O 2 ) and organic hydroperoxides and the activity of glutathione peroxidase GPx increased in response to vitamin E treatment Srikanta et al (2012).…”

Section: Introductionmentioning

confidence: 99%

Factors Those Up Regulate <i>Klotho</i> and Glutathione Peroxidase-1 Gene Expression Improve Renal Function in Rats with Acute Renal Failure

Elgendey¹,

Hemeda²,

Sosa³

et al. 2015

American Journal of Biochemistry and Biotechnology

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Acute Renal Failure (ARF) has traditionally been defined as the abrupt and progressive loss of kidney functions resulting in the retention of urea and other nitrogenous waste products associated with interstitial inflammation, tubular injury and increasing Tumor Necrosis Factor (TNF). Mortality in patients with ARF remains high >50% in severely ill patients. Klotho gene is a new anti-aging gene. Genetic mutation of klotho gene causes multiple premature aging-like phenotypes and shortens lifespan. Klotho gene is highly expressed in the kidney and a soluble form of klotho functions as an endocrine substance that exerts multiple actions including the modulation of renal solute transport and the protection of the kidney. This study aimed to clarify the pre treatment and/or post treatment effect of vitamin E as an antioxidant on kidney functions, klotho gene expression and glutathione peroxidase-1 gene expression among rats with acute renal failure. Using glycerol as oxidative stress factor to cause acute renal failure and Real time PCR for assessment of gene expression of target gene in the control and treated groups. Our results demonstrated that the vitamin E (α tocopherol) as antioxidant factor decreased the kidney injuries as pre renal failure administer and improve kidney function as post renal failure administer. Those effects were through up regulating the Klotho as anti aging gene and the Glutathione Peroxidase (GPx-1) as antioxidant gene expression in the kidney tissue. We concluded that factors those up regulate the klotho gene expression can use as protective factors against kidney injuries and to improve kidney function in renal failure.

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