Giovana R. Punaro
Federal University of São Paulo
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Publication
Featured researches published by Giovana R. Punaro.
Nitric Oxide | 2014
Giovana R. Punaro; Fabiane R. Maciel; Adelson M. Rodrigues; Marcelo Macedo Rogero; Cristina S.B. Bogsan; Maricê Nogueira de Oliveira; Silvia Saiuli Miki Ihara; Sergio R. R. Araujo; Talita Rojas Sanches; Lúcia Andrade; Elisa Mieko Suemitsu Higa
This study aimed at assessing the effects of Kefir, a probiotic fermented milk, on oxidative stress in diabetic animals. The induction of diabetes was achieved in adult male Wistar rats using streptozotocin (STZ). The animals were distributed into four groups as follows: control (CTL); control Kefir (CTLK); diabetic (DM) and diabetic Kefir (DMK). Starting on the 5th day of diabetes, Kefir was administered by daily gavage at a dose of 1.8 mL/day for 8 weeks. Before and after Kefir treatment, the rats were placed in individual metabolic cages to obtain blood and urine samples to evaluate urea, creatinine, proteinuria, nitric oxide (NO), thiobarbituric acid reactive substances (TBARS) and C-reactive protein (CRP). After sacrificing the animals, the renal cortex was removed for histology, oxidative stress and NOS evaluation. When compared to CTL rats, DM rats showed increased levels of glycemia, plasmatic urea, proteinuria, renal NO, superoxide anion, TBARS, and plasmatic CRP; also demonstrated a reduction in urinary urea, creatinine, and NO. However, DMK rats showed a significant improvement in most of these parameters. Despite the lack of differences observed in the expression of endothelial NO synthase (eNOS), the expression of inducible NO synthase (iNOS) was significantly lower in the DMK group when compared to DM rats, as assessed by Western blot analysis. Moreover, the DMK group presented a significant reduction of glycogen accumulation within the renal tubules when compared to the DM group. These results indicate that Kefir treatment may contribute to better control of glycemia and oxidative stress, which is associated with the amelioration of renal function, suggesting its use as a non-pharmacological adjuvant to delay the progression of diabetic complications.
Life Sciences | 2017
Clemerson S. Oliveira; Adelson M. Rodrigues; Guilherme B. Nogueira; Marcos A. Nascimento; Giovana R. Punaro; Elisa Ms Higa
Introduction: Acute kidney injury is a serious public health problem, especially in intensive care units, where patients may require dialysis support, resulting in 50% mortality. Aim: To evaluate the effects of moderate aerobic exercise on the recovery phase of acute kidney injury induced by gentamicin in rats. Main methods: Male adult Wistar rats were allocated into 4 groups: W10 + R30, G10 + R30, W10 + EX30 and G10 + EX30; W10 received water (gentamicin vehicle) and G10 received gentamicin for 10 days; R30 remained resting and EX30 made exercise for 30 days after gentamicin suspension. Training was performed on treadmill. Blood, 24 h urine and kidneys were collected for renal function and oxidative stress, antioxidant, TGF‐&bgr; and histological analysis. Key findings: Gentamicin treatment caused decreased renal function significant oxidative stress, reduced urinary nitric oxide and increased TGF‐&bgr;. G10 + R30 presented partial recovery of metabolic data, renal function and lipoperoxidation levels, although they were still altered compared to W10 + R30. Besides, we observed the presence of lymphomononuclear infiltrate in the kidneys of G10 + R30. G10 + EX30 vs G10 + R30 showed additional improvement of all the mentioned parameters, showing at histology, regeneration of the tubule epithelium. Significance: Our data suggest that moderate exercises could help in the recovery of metabolic parameters, renal function and structure on gentamicin‐induced AKI, perhaps due to restoration of redox balance. This could protect the kidneys from further insults like challenges with nephrotoxic drugs or the aging per se.
Experimental Gerontology | 2017
Deborah Seraphim; Giovana R. Punaro; Thamires de Oliveira Fernandes; Milton Ginoza; Guiomar Silva Lopes; Elisa Mieko Suemitsu Higa
ABSTRACT The aging process is a complex phenomenon that leads the body to several changes, affecting its integrity and resulting in chronic pathologies, which compromises health and quality of life of elderly people. Animals supplemented with fructose have been used as an experimental model for induction of insulin resistance. The objective of this study was to evaluate the metabolic effects and the levels of oxidative/nitrosative stress in the kidney of senescent rats with a high fructose intake. The animals were allocated into 4 groups: young control (Y), aged control (A), young fructose (YF) and aged fructose (AF). Groups Y and A received water and groups YF and AF received fructose (100 g/L) in the water, both ad libitum. After 12 weeks of high fructose intake, the animals were sacrificed to collect their kidneys, blood and the thoracic aorta. The results are presented as mean ± SE, analyzed by the One‐Way ANOVA test with Newman‐Keuls post‐test; significant at p < 0.05. The fructose overload caused metabolic dysfunctions and insulin resistance, confirming the efficacy of the chosen model. In this study, we observed a body weight gain in the studied groups (except in the elderly fructose group), and an increase in general caloric intake, diuresis and adipose tissue; insulin resistance, increased fasting glucose, triglycerides and cholesterol in the fructose groups. We also found a loss of renal function, increased oxidative/nitrosative stress and inflammation, and a reduction of antioxidants and a lower vasodepressor response in the studied groups, especially those who consumed fructose. In summary, our data showed that aging or high fructose intake contributed to the increase of oxidative/nitrosative stress in animals, demonstrating that at the dose and the period of fructose treatment utilized in this study, fructose was not able to aggravate several aspects which were already altered by aging. We believe that the high fructose intake simulates most of the effects of aging, and this understanding would be useful to prevent or minimize many of the alterations caused by this condition. HighlightsAging or high fructose intake contributes to an increased oxidative/nitrosative stress, and inflammation.High fructose intake reduced vasodilatation response in young and aging female rats.High fructose intake simulates most of the effects of aging.
PLOS ONE | 2014
Adelson M. Rodrigues; Cassia Toledo Bergamaschi; Maria José da Silva Fernandes; Edgar J. Paredes-Gamero; Marcus V. Curi; Alice T. Ferreira; Sergio R. R. Araujo; Giovana R. Punaro; Fabiane R. Maciel; Guilherme B. Nogueira; Elisa Mieko Suemitsu Higa
Clinical Nutrition | 2016
Fabiane R. Maciel; Giovana R. Punaro; Adelson M. Rodrigues; Cristina S.B. Bogsan; Marcelo Macedo Rogero; Maricê Nogueira de Oliveira; Margaret Gori Mouro; Elisa Mieko Suemitsu Higa
Clinical nutrition ESPEN | 2017
Marcos A. Nascimento; F. S. Lira; Giovana R. Punaro; Marco Túlio de Mello; Sergio Tufik; Elisa Mieko Suemitsu Higa
Purinergic Signalling | 2018
Adelson M. Rodrigues; R. S. Serralha; C. Farias; Giovana R. Punaro; Maria José da Silva Fernandes; Elisa Mieko Suemitsu Higa
Nitric Oxide | 2018
Guilherme B. Nogueira; Giovana R. Punaro; Clemerson S. Oliveira; Fabiane R. Maciel; Thamires de Oliveira Fernandes; Deyse Y. Lima; Adelson M. Rodrigues; Margaret Gori Mouro; Sergio R. R. Araujo; Elisa Mieko Suemitsu Higa
Free Radical Biology and Medicine | 2017
Adelson M. Rodrigues; Robson S Serralha; Maria José da Silva Fernandes; Giovana R. Punaro; Elisa Ms Higa
Clinical Nutrition | 2017
Giovana R. Punaro; Deyse Y. Lima; Adelson M. Rodrigues; Samuel Pugliero; Margaret Gori Mouro; Marcelo Macedo Rogero; Elisa Mieko Suemitsu Higa