scholarly journals A review of oxidative stress in acute kidney injury: protective role of medicinal plants-derived antioxidants

2013 ◽  
Vol 10 (4) ◽  
Author(s):  
S Palipoch
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Medicinal Plants ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Stanniocalcin-1 Alleviates Contrast-Induced Acute Kidney Injury by Regulating Mitochondrial Quality Control via the Nrf2 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Fei Zhao ◽  
Li-Xin Feng ◽  
Qian Liu ◽  
Hong-Shen Wang ◽  
Cheng-Yuan Tang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Quality Control ◽  
Kidney Injury ◽  
Protective Role ◽  
Mitochondrial Quality Control ◽  
Therapy Strategy ◽  
Nrf2 Signaling Pathway ◽  
Short And Long Term ◽  
Renal Tubular

Contrast-induced acute kidney injury (CI-AKI) is the third common cause of acute kidney injury (AKI), which is associated with poor short- and long-term outcomes. Currently, effective therapy strategy for CI-AKI remains lacking. Stanniocalcin-1 (STC1) is a conserved glycoprotein with antiapoptosis and anti-inflammatory functions, but the role of STC1 in controlling CI-AKI is unknown. Here, we demonstrated a protective role of STC1 in contrast-induced injury in cultured renal tubular epithelial cells and CI-AKI rat models. Recombinant human STC1 (rhSTC1) regulated mitochondrial quality control, thus suppressing contrast-induced mitochondrial damage, oxidative stress, inflammatory response, and apoptotic injury. Mechanistically, activation of the Nrf2 signaling pathway contributes critically to the renoprotective effect of STC1. Together, this study demonstrates a novel role of STC1 in preventing CI-AKI and reveals Nrf2 as a molecular target of STC1. Therefore, this study provides a promising preventive target for the treatment of CI-AKI.

Protective role of HO‐1 against acute kidney injury caused by cutaneous exposure to arsenicals

2020 ◽  
Vol 1480 (1) ◽  
pp. 155-169
Author(s):  
Ritesh K. Srivastava ◽  
Suhail Muzaffar ◽  
Jasim Khan ◽  
Amie M. Traylor ◽  
Jaroslaw W. Zmijewski ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Protective role of fructokinase blockade in the pathogenesis of acute kidney injury in mice

2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Ana Andres-Hernando ◽  
Nanxing Li ◽  
Christina Cicerchi ◽  
Shinichiro Inaba ◽  
Wei Chen ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Protective Effect of Procambarus Clarkia Hemolymph against Acute Kidney Injury Induced by Gentamicin in Rats

2020 ◽  
pp. 123-129
Author(s):  
Abdeljalil M`ohamed Al Shawoush ◽  
Ayman Saber Mohamed ◽  
Sohair Ramadan Fahmy
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role ◽  
Pharmacological Activities ◽  
Partial Restoration ◽  
Stress Markers ◽  
Study Results ◽  
Liver Functions ◽  
Kidney Functions

Background: P.clarkii hemolymph has several pharmacological activities against inflammation, bacteria and tumor. The current study aimed to explore the efficacy of P.clarkii hemolymph against the renal toxicity induced by Gentamicin (GM) in rats. Methods: The animals were divided randomly into three groups (six per group): control, GM and P.clarkii. Tissues toxicity was established after injection of GM daily for eight days at a dose 100 mg/kg. Kidney functions, liver functions, oxidative stress markers and histopathology of tissues were investigated in the study. Results: P.clarkii treated rats showed a significant decrease in urea, creatinine, uric acid, ALT, AST, and MDA levels while GSH and CAT levels increased. The histology of kidney investigation showed partial restoration of renal architecture. Conclusion: The study results revealed the protective role of p.clarkii hemolymph against gentamicin-induced acute kidney injury in rats.

The protective role of macrophage migration inhibitory factor in acute kidney injury after cardiac surgery

2018 ◽  
Vol 10 (441) ◽  
pp. eaan4886 ◽  
Author(s):  
Christian Stoppe ◽  
Luisa Averdunk ◽  
Andreas Goetzenich ◽  
Josefin Soppert ◽  
Arnaud Marlier ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Kidney Injury ◽  
Protective Role ◽  
Inhibitory Factor ◽  
Macrophage Migration

The protective role of estrogen and its receptors in gentamicin-induced acute kidney injury in rats

Life Sciences ◽  
2019 ◽  
Vol 239 ◽  
pp. 117082
Author(s):  
Sayed M. Abd El-Lateef ◽  
El-Sayed M. El-Sayed ◽  
Ahmed M. Mansour ◽  
Salama A. Salama
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Protective Role

scholarly journals Protective role of endothelial calpain knockout in lipopolysaccharide-induced acute kidney injury via attenuation of the p38-iNOS pathway and NO/ROS production

2020 ◽  
Vol 52 (4) ◽  
pp. 702-712
Author(s):  
Zhifeng Liu ◽  
Jingjing Ji ◽  
Dong Zheng ◽  
Lei Su ◽  
Tianqing Peng ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Caspase 3 ◽  
Kidney Injury ◽  
Protective Role ◽  
Inos Expression ◽  
Calpain Inhibitor ◽  
Ros Production ◽  
Enos Expression ◽  
Cellular Apoptosis

Abstract To explore the role of calpain and its signaling pathway in lipopolysaccharide (LPS)-induced acute kidney injury (AKI), animal models of endotoxemia were established by administration of LPS to mice with endothelial-specific Capn4 knockout (TEK/Capn4−/−), mice with calpastatin (an endogenous calpain inhibitor) overexpression (Tg-CAST) and mice with myeloid-specific Capn4 knockout (LYZ/Capn4−/−). Mouse pulmonary microvascular endothelial cells (PMECs) were used as a model of the microvascular endothelium and were stimulated with LPS. Renal function, renal inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) expression, cellular apoptosis, plasma and renal levels of NO and reactive oxygen species (ROS), and phosphorylation of mitogen-activated protein kinase (MAPK) family members (p38, ERK1/2, and JNK1/2) were examined. Moreover, a calpain inhibitor, calpastatin overexpression adenoviruses and MAPK inhibitors were used. Significant renal dysfunction was induced by LPS stimulation, and recovery was observed in TEK/Capn4−/− and Tg-CAST mice but not in LYZ/Capn4−/− mice. Endothelial Capn4 knockout also abrogated the LPS-induced increases in renal iNOS expression, caspase-3 activity and apoptosis and plasma and renal NO and ROS levels but did not obviously affect renal eNOS expression. Moreover, LPS increased both calpain and caspase-3 activity, and only the expression of iNOS in PMECs was accompanied by increased phosphorylation of p38 and JNK. Inhibiting calpain activity or p38 phosphorylation alleviated the increased iNOS expression, NO/ROS production, and cellular apoptosis induced by LPS. These results suggest that endothelial calpain plays a protective role in LPS-induced AKI by inhibiting p38 phosphorylation, thus attenuating iNOS expression and further decreasing NO and ROS overproduction-induced endothelial apoptosis.

A protective role of unfolded protein response in mouse ischemic acute kidney injury

2008 ◽  
Vol 592 (1-3) ◽  
pp. 138-145 ◽  
Author(s):  
Worapat Prachasilchai ◽  
Hiroko Sonoda ◽  
Naoko Yokota-Ikeda ◽  
Sayaka Oshikawa ◽  
Chie Aikawa ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Unfolded Protein Response ◽  
Kidney Injury ◽  
Protective Role ◽  
Unfolded Protein ◽  
Ischemic Acute Kidney Injury ◽  
Protein Response

scholarly journals Protective role of DJ-1 in endotoxin-induced acute kidney injury

2020 ◽  
Vol 319 (4) ◽  
pp. F654-F663 ◽  
Author(s):  
Joseph Leeds ◽  
Yogesh Scindia ◽  
Valentina Loi ◽  
Ewa Wlazlo ◽  
Elizabeth Ghias ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Collecting Duct ◽  
Kidney Injury ◽  
Protective Role ◽  
In Vivo Model ◽  
Renal Tubules ◽  
Death Domain ◽  
Renal Tubular

Acute kidney injury (AKI) is a frequent complication of sepsis and an important cause of morbidity and mortality worldwide. A cornerstone of sepsis-associated AKI is dysregulated inflammation, leading to increased tissue oxidative stress and free radical formation, which leads to multiple forms of cell death. DJ-1 is a peroxiredoxin protein with multiple functions, including its ability to control cellular oxidative stress. Although DJ-1 is expressed prominently by renal tubules, its role in AKI has not been investigated. In the present study, we examined the effect of DJ-1 deficiency in a murine model of endotoxin-induced AKI. Endotoxemia induced greater kidney injury in DJ-1-deficient mice. Furthermore, DJ-1 deficiency increased renal oxidative stress associated with increased renal tubular apoptosis and with expression of death domain-associated protein (DAXX). Similar to the in vivo model, in vitro experiments using a medullary collecting duct cell line (mIMCD3) and cytotoxic serum showed that serum obtained from wild-type mice resulted in increased expression of s100A8/s100A9, DAXX, and apoptosis in DJ-1-deficient mIMCD3 cells. Our findings demonstrate a novel renal protective role for renal tubular DJ-1 during endotoxemia through control of oxidative stress, renal inflammation, and DAXX-dependent apoptosis.

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