scholarly journals Cadmium-Induced Kidney Injury in Mice Is Counteracted by a Flavonoid-Rich Extract of Bergamot Juice, Alone or in Association with Curcumin and Resveratrol, via the Enhancement of Different Defense Mechanisms

Biomedicines ◽  
2021 ◽  
Vol 9 (12) ◽  
pp. 1797
Author(s):  
Santa Cirmi ◽  
Alessandro Maugeri ◽  
Antonio Micali ◽  
Herbert Ryan Marini ◽  
Domenico Puzzolo ◽  
...  
Keyword(s):  
Defense Mechanisms ◽  
Kidney Injury ◽  
Environmental Toxicants ◽  
Therapeutic Approaches ◽  
Renal Functions ◽  
Main Target ◽  
Potential Strategy ◽  
Cd Exposure ◽  
Morphometric Evaluation ◽  
Gpx Activity

Cadmium (Cd) represents a public health risk due to its non-biodegradability and long biological half-life. The main target of Cd is considered the kidney, where it accumulates. No effective treatment for Cd poisoning is available so that several therapeutic approaches were proposed to prevent damages after Cd exposure. We evaluated the effects of a flavonoid-rich extract of bergamot juice (BJe), alone or in association with curcumin (Cur) and resveratrol (Re), in the kidney of mice exposed to cadmium chloride (CdCl2). Male mice were administered with CdCl2 and treated with Cur, Re, or BJe alone or in combination for 14 days. The kidneys were processed for biochemical, structural and morphometric evaluation. Cd treatment significantly increased urea nitrogen and creatinine levels, along with tp53, Bax, Nos2 and Il1b mRNA, while reduced that of Bcl2, as well as glutathione (GSH) content and glutathione peroxidase (GPx) activity. Moreover, Cd caused damages to glomeruli and tubules, and increased Nrf2, Nqo1 and Hmox1 gene expression. Cur, Re and BJe at 40 mg/kg significantly improved all parameters, while BJe at 20 mg/kg showed a lower protective effect. After treatment with the associations of the three nutraceuticals, all parameters were close to normal, thus suggesting a new potential strategy in the protection of renal functions in subjects exposed to environmental toxicants.

scholarly journals Endotoxin Effects on Cardiac and Renal Functions and Cardiorenal Syndromes

2017 ◽  
Vol 44 (4) ◽  
pp. 314-326 ◽  
Author(s):  
Grazia Maria Virzì ◽  
Anna Clementi ◽  
Alessandra Brocca ◽  
Claudio Ronco
Keyword(s):  
Immune Cells ◽  
Early Identification ◽  
Kidney Injury ◽  
Therapeutic Approaches ◽  
Gram Negative ◽  
Renal Functions ◽  
Cycle Arrest ◽  
Critical Ill Patients ◽  
Cellular Apoptosis

Gram-negative sepsis is a major cause of morbidity and mortality in critical ill patients. Recent findings in molecular biology and in signaling pathways have enhanced our understanding of its pathogenesis and opened up opportunities of innovative therapeutic approaches. Endotoxin plays a pivotal role in the pathogenesis of multi-organ dysfunction in the setting of gram-negative sepsis. Indeed, heart and kidney impairments seem to be induced by the release of circulating pro-inflammatory and pro-apoptotic mediators triggered by endotoxin interaction with immune cells. These molecules are responsible for cellular apoptosis, autophagy, cell cycle arrest, and microRNAs activation. Therefore, the early identification of sepsis-associated acute kidney injury and heart dysfunction may improve the patient clinical outcome. In this report, we will consider the role of endotoxin in the pathogenesis of sepsis, its effects on both cardiac and renal functions, and the interactions between these 2 systems in the setting of cardiorenal syndromes (CRS), particularly in CRS type 5. Finally, we will discuss the possible role of extracorporeal therapies in reducing endotoxin levels.

scholarly journals The Potential Use of Vitamin C to Prevent Kidney Injury in Patients with COVID-19

Diseases ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 46
Author(s):  
Feng Xu ◽  
Yawei Wen ◽  
Xinge Hu ◽  
Tiannan Wang ◽  
Guoxun Chen
Keyword(s):  
Vitamin C ◽  
Distress Syndrome ◽  
Kidney Injury ◽  
Mortality Rates ◽  
Protective Effects ◽  
Global Public Health ◽  
Health Crisis ◽  
Public Health Crisis ◽  
Renal Functions ◽  
Potential Use

The newly found SARS-CoV-2 has led to the pandemic of COVID-19, which has caused respiratory distress syndrome and even death worldwide. This has become a global public health crisis. Unfortunately, elders and subjects with comorbidities have high mortality rates. One main feature of COVID-19 is the cytokine storm, which can cause damage in cells and tissues including the kidneys. Here, we reviewed the current literature on renal impairments in patients with COVID-19 and analyzed the possible etiology and mechanisms. In addition, we investigated the potential use of vitamin C for the prevention of renal injury in those patients. It appears that vitamin C could be helpful to improve the outcomes of patients with COVID-19. Lastly, we discussed the possible protective effects of vitamin C on renal functions in COVID-19 patients with existing kidney conditions.

scholarly journals Effect of alpha-lipoic acid on antioxidant gene expression and kidney injury in alloxan-induced diabetic rats

2018 ◽  
Vol 8 (1) ◽  
pp. 6-6 ◽  
Author(s):  
Parisa Jamor ◽  
Hassan Ahmadvand ◽  
Hesam Ashoory ◽  
Esmaeel Babaeenezhad
Keyword(s):  
Gene Expression ◽  
Lipoic Acid ◽  
Kidney Injury ◽  
Diabetic Rats ◽  
Pcr Analysis ◽  
Control Group ◽  
Diabetic Patients ◽  
Alpha Lipoic Acid ◽  
The Impact ◽  
Gpx Activity

Background: Myeloperoxidase (MPO) is involved in the initiation, progression, and complications of atherosclerosis in diabetic patients. Objectives: In the current study, the impact of alpha-lipoic acid (LA), a natural antioxidant and a cofactor in the enzyme complexes on MPO, catalase (CAT) and glutathione peroxidase (GPx) activity, glutathione (GSH) and malondialdehyde (MDA) level, histopathology of kidney and expression of antioxidant enzymes, superoxide dismutase (SOD), GPx and CAT which are involved in the detoxification of reactive oxygen species (ROS), was evaluated in alloxan-induced diabetic rats. Materials and Methods: In this study, 30 male Rattus norvegicus rats randomly divided into three groups; control (C), non-treated diabetic (NTD), and LA-treated diabetics (LATD) was induced by alloxan monohydrate (100mg/kg; subcutaneous [SC]). Then treatment was performed with alphaLA (100 mg/kg intraperitoneal (i.p) daily to 6 weeks). Blood sample of animals collected to measure levels of MPO, CAT and GPx activity GSH and MDA. Kidney paraffin sections were prepared to estimate histological studies and to measure quantitative gene expression SOD, GPX and CAT in kidney. Results: Induction of diabetes led to a significant increase in MPO and MDA, reduced GSH level and GPx and CAT activities (P < 0.05). However, treatment with alpha-LA led to a significant elevation in GPx, CAT and GSH levels with a reduction in MPO activities and MDA levels (P < 0.05). Furthermore, the real-time reverse transcriptase-polymerase chain reaction (RT-PCR) analysis results showed increased expressions of GPx, CAT and SOD enzyme in the treatment group compared with the diabetic control group. Histopathological lesions such as increased glomerular volume and lymphocyte infiltration were attenuated in the alpha-LA treated group. Conclusions: Our findings indicated that alpha-LA supplementation is effective in preventing complications induced by oxidative stress and atherosclerosis in diabetic rats.

scholarly journals Autophagy Function and Regulation in Kidney Disease

Biomolecules ◽  
2020 ◽  
Vol 10 (1) ◽  
pp. 100 ◽  
Author(s):  
Gur P. Kaushal ◽  
Kiran Chandrashekar ◽  
Luis A. Juncos ◽  
Sudhir V. Shah
Keyword(s):  
Cell Death ◽  
Renal Injury ◽  
Mammalian Target Of Rapamycin ◽  
Kidney Injury ◽  
Therapeutic Approaches ◽  
Regulated Necrosis ◽  
Atg Genes ◽  
Cellular Components ◽  
The Impact

Autophagy is a dynamic process by which intracellular damaged macromolecules and organelles are degraded and recycled for the synthesis of new cellular components. Basal autophagy in the kidney acts as a quality control system and is vital for cellular metabolic and organelle homeostasis. Under pathological conditions, autophagy facilitates cellular adaptation; however, activation of autophagy in response to renal injury may be insufficient to provide protection, especially under dysregulated conditions. Kidney-specific deletion of Atg genes in mice has consistently demonstrated worsened acute kidney injury (AKI) outcomes supporting the notion of a pro-survival role of autophagy. Recent studies have also begun to unfold the role of autophagy in progressive renal disease and subsequent fibrosis. Autophagy also influences tubular cell death in renal injury. In this review, we reported the current understanding of autophagy regulation and its role in the pathogenesis of renal injury. In particular, the classic mammalian target of rapamycin (mTOR)-dependent signaling pathway and other mTOR-independent alternative signaling pathways of autophagy regulation were described. Finally, we summarized the impact of autophagy activation on different forms of cell death, including apoptosis and regulated necrosis, associated with the pathophysiology of renal injury. Understanding the regulatory mechanisms of autophagy would identify important targets for therapeutic approaches.

scholarly journals Perioperative Organ Injury

2013 ◽  
Vol 119 (6) ◽  
pp. 1474-1489 ◽  
Author(s):  
Karsten Bartels ◽  
Jörn Karhausen ◽  
Eric T. Clambey ◽  
Almut Grenz ◽  
Holger K. Eltzschig
Keyword(s):  
Distress Syndrome ◽  
Kidney Injury ◽  
Organ Injury ◽  
Therapeutic Approaches ◽  
The Past ◽  
Novel Treatment ◽  
Current Review ◽  
Common Causes ◽  
Treatment Concepts ◽  
Insight Into

Abstract Despite the fact that a surgical procedure may have been performed for the appropriate indication and in a technically perfect manner, patients are threatened by perioperative organ injury. For example, stroke, myocardial infarction, acute respiratory distress syndrome, acute kidney injury, or acute gut injury are among the most common causes for morbidity and mortality in surgical patients. In the current review, the authors discuss the pathogenesis of perioperative organ injury, and provide select examples for novel treatment concepts that have emerged over the past decade. Indeed, the authors are of the opinion that research to provide mechanistic insight into acute organ injury and identification of novel therapeutic approaches for the prevention or treatment of perioperative organ injury represent the most important opportunity to improve outcomes of anesthesia and surgery.

An age-related difference in hyperoxia lethality: role of lung antioxidant defense mechanisms

1995 ◽  
Vol 268 (4) ◽  
pp. L539-L545 ◽  
Author(s):  
A. T. Canada ◽  
L. A. Herman ◽  
S. L. Young
Keyword(s):  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Fischer 344 Rats ◽  
Fischer 344 ◽  
Related Difference ◽  
Age Related ◽  
65 H ◽  
Old Rats ◽  
Gpx Activity

The role of animal age in the lethal response to > 98% oxygen has been extensively studied, with the observation that neonatal rats were resistant while mature animals were sensitive. Antioxidant enzymes increased during the oxygen exposure in neonatal but not in mature rats, suggesting they were important in the age-related toxicity difference. Because no studies had compared the response of mature and old rats to hyperoxia, we exposed Fischer 344 rats, aged 2 and 27 mo, to > 98% oxygen. Unexpectedly, the old rats lived significantly longer than young, 114 and 65 h, respectively. No histopathological differences were found to explain the results. Of the antioxidants, only glutathione peroxidase (GPx) activity was higher in the lungs of nonexposed old rats. Superoxide dismutase (SOD) was higher in the young, results opposite those expected if SOD was important in the lethality difference. No antioxidant induction occurred in the old oxygen-exposed rats. These results suggest that although there may be a role for GPx, mechanisms in addition to antioxidant protection and inflammation are likely responsible for the age-related difference in hyperoxia lethality.

scholarly journals Cardioprotective Effect of Quercetin in 5/6-Nephrectomized Rats: Focus on Myocardial fibrosis and Oxidative Stress

2017 ◽  
Vol 2 (3) ◽  
pp. 87-95
Author(s):  
Tri Yuliani ◽  
Melva Louisa ◽  
Wawaimuli Arozal ◽  
Vivian Soetikno ◽  
Nafrialdi Nafrialdi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Fibrosis ◽  
Defense Mechanisms ◽  
Chronic Administration ◽  
Cardioprotective Effect ◽  
Sprague Dawley ◽  
Antioxidant Mechanism ◽  
Uremic Cardiomyopathy ◽  
And Oxidative Stress ◽  
Gpx Activity

Uremic cardiomyopathy is the leading cause of death in patients with chronic kidney disease. Fluid overload and oxidative stress play important roles in its pathogenesis. This study aims to determine the effect of quercetin on uremic cardiomyopathy in 5/6-nephrectomized rats. To our knowledge, its cardioprotective effect on uremic cardiomyopathy induced in rats by 5/6 nephrectomy has not been investigated yet. Uremia was induced surgically in male Sprague-Dawley rats via 5/6 nephrectomy. Quercetin was administered per orally at a dose of 100 mg/kg/day for 8 weeks prior to sacrifice. Meanwhile, captopril was administered at a dose of 10 mg/kg/day. Lipid peroxidation was assessed using TBARS reaction, while GPX activity was determined to explore the endogen antioxidant mechanism. Myocardial fibrosis was analyzed using Massons’ Trichrome staining and the level of NT-proBNP in plasma was measured as a marker of cardiac dysfunction. Nephrectomy 5/6 had no effects on plasma NT– proBNP levels, cardiac and plasma MDA levels, but induced mild myocardial fibrosis and significant increase in cardiac GPX activity in comparison with normal rat (p<0.05). However, administration of quercetin or captopril did not ameleriote those mild myocardial fibrosis and increased GPX activity. Uremic cardiomyopathy induced by 5/6 nephrectomy demonstrated mild myocardial fibrosis but preservation of cardiac function demonstrated by NT-proBNP levels. Increased of GPX activity in the nephrectomized-rats compared to the control rats (p<0.05) suggests induction of antioxidant defense mechanisms that might not be exhausted yet. This condition highlighted a compensatory phase which was unchanged following chronic administration of either quercetin or captopril.

scholarly journals The Application of 99mTc-DTPA Renal Dynamic Imaging to Measuring Renal Function of Children with Acute Lymphoblastic Leukemia after Induction Therapy

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Lidan Wang ◽  
Kailan Chen ◽  
Qiong Xu
Keyword(s):  
Renal Function ◽  
Acute Lymphoblastic Leukemia ◽  
Induction Therapy ◽  
Estimated Glomerular Filtration Rate ◽  
Lymphoblastic Leukemia ◽  
Kidney Injury ◽  
Binary Logistic Regression ◽  
Dynamic Imaging ◽  
High Dose ◽  
Renal Functions

Purpose. The study was aimed at assessing renal functions of children with acute lymphoblastic leukemia (ALL) after induction therapy by 99mTc-DTPA renal dynamic imaging Gates method (GFRGates) and investigating whether renal function after induction therapy will affect the occurrence of high-dose methotrexate- (HDMTX-) induced acute kidney injury (AKI). Methods. Children with newly diagnosed ALL were enrolled. Renal functions before the administration of HDMTX were assessed by estimated glomerular filtration rate (eGFR) and GFRGates, respectively, before the first cycle of HDMTX after induction therapy. The areas under the ROC curve were used to assess covariates’ ability to predict HDMTX-induced AKI. Results. 102 children with ALL were included in the study. A stepwise backward binary logistic regression showed that only standardized GFRGates was an independent risk factor for HDMTX-induced AKI ( p = 0.018 , odds ratio 0.985, 95% CI 0.972-0.997). The area under the ROC of standardized GFRGates was 0.679 ( p = 0.012 , 95% CI 0.554-0.804). Conclusion. Standardized GFRGates showed that the normal renal function of children is not enough to be used as a cutoff point to predict HDMTX-induced AKI in ALL children receiving HDMTX. More attention and supportive care should be given to the children with standardized GFRGates lower than the cutoff value to avoid the HDMTX-induced AKI.

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