scholarly journals Protective effects of protocatechuic acid against cisplatin-induced renal damage in rats

2015 ◽  
Vol 19 ◽  
pp. 20-27 ◽  
Author(s):  
Noriko Yamabe ◽  
Jun Yeon Park ◽  
Seungyong Lee ◽  
Eun-Ju Cho ◽  
Sanghyun Lee ◽  
...  
Keyword(s):  
Renal Damage ◽  
Protocatechuic Acid ◽  
Protective Effects

Protective effects of fraction 4a of polysaccharides isolated from Lycium barbarum against KBrO3-induced renal damage in rats

2017 ◽  
Vol 8 (7) ◽  
pp. 2566-2572 ◽  
Author(s):  
J. Li ◽  
M. Shi ◽  
B. Ma ◽  
Y. Zheng ◽  
R. Niu ◽  
...  
Keyword(s):  
Oxidation Resistance ◽  
Renal Damage ◽  
Protective Effects ◽  
Renal Cells ◽  
Lycium Barbarum

LBP-4a exhibits protective effects on KBrO3-induced renal damage, and the mechanism correlates with the increase of oxidation resistance in renal cells.

scholarly journals Correction to: Heat stress-induced renal damage in poultry and the protective effects of HSP60 and HSP47

2020 ◽  
Vol 25 (2) ◽  
pp. 379-379
Author(s):  
Shu Tang ◽  
Shuang Zhou ◽  
Bin Yin ◽  
Jiao Xu ◽  
Liangjiao Di ◽  
...  
Keyword(s):  
Heat Stress ◽  
Renal Damage ◽  
Protective Effects

scholarly journals Heat stress-induced renal damage in poultry and the protective effects of HSP60 and HSP47

2018 ◽  
Vol 23 (5) ◽  
pp. 1033-1040 ◽  
Author(s):  
Shu Tang ◽  
Shuang Zhou ◽  
Bin Yin ◽  
Jiao Xu ◽  
Liangjiao Di ◽  
...  
Keyword(s):  
Heat Stress ◽  
Renal Damage ◽  
Protective Effects

Protective Effects of Serotonin and its Derivatives, N-Feruloylserotonin and N-(p-Coumaroyl) Serotonin, Against Cisplatin-Induced Renal Damage in Mice

2019 ◽  
Vol 47 (02) ◽  
pp. 369-383 ◽  
Author(s):  
Chan Hum Park ◽  
Ah Young Lee ◽  
Ji Hyun Kim ◽  
Su Hui Seong ◽  
Eun Ju Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Renal Damage ◽  
Pleiotropic Effect ◽  
Protective Effects ◽  
Related Protein ◽  
Renoprotective Effect ◽  
Serotonin Derivatives ◽  
Mitogen Activated Protein ◽  
Apoptosis Related Protein

This study examined whether serotonin and two of its derivatives, [Formula: see text]-feruloylserotonin and [Formula: see text]-([Formula: see text]-coumaroyl) serotonin, have a renoprotective effect in a mouse model of cisplatin-induced acute renal failure. Cisplatin (20[Formula: see text]mg/kg body weight) was administered by intraperitoneal injection to male BALB/c mice that had received oral serotonin, [Formula: see text]-feruloylserotonin or [Formula: see text]-([Formula: see text]-coumaroyl) serotonin (7.5[Formula: see text]mg/kg body weight per day) during the preceding 2 days. At 3 days after the cisplatin injection, serum and renal biochemical factors, oxidative stress, inflammation and apoptosis-related protein expression were evaluated, and histological examinations were performed. Cisplatin caused reduction in body weight and an increase in kidney weight; however, [Formula: see text]-([Formula: see text]-coumaroyl) serotonin and [Formula: see text]-feruloylserotonin attenuated these effects. Moreover, the serotonin derivatives significantly decreased serum urea nitrogen and creatinine levels. They also significantly reduced the level of reactive oxygen species and upregulated the expression of glutathione peroxidase in the kidney. Furthermore, the serotonin derivatives improved the abnormal expression of mitogen-activated protein kinases activation-dependent inflammation- and apoptosis-related protein and caused less renal damage. These results provide important evidence that [Formula: see text]-([Formula: see text]-coumaroyl) serotonin and [Formula: see text]-feruloylserotonin exert a pleiotropic effect on several parameters related to oxidative stress, inflammation and apoptosis. The derivatives also have a renoprotective effect in cisplatin-treated mice; however, this effect is higher with [Formula: see text]-([Formula: see text]-coumaroyl) serotonin.

scholarly journals Protective Effects of Recombinant Human Soluble Thrombomodulin on Lipopolysaccharide-Induced Acute Kidney Injury

2020 ◽  
Vol 21 (7) ◽  
pp. 2519
Author(s):  
Yuji Nozaki ◽  
Jinhai Ri ◽  
Kenji Sakai ◽  
Kaoru Niki ◽  
Masanori Funauchi ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Damage ◽  
Cell Activation ◽  
Therapeutic Strategy ◽  
Cytokine Production ◽  
Kidney Injury ◽  
Protective Effects ◽  
Inflammatory Cytokine Production ◽  
Soluble Thrombomodulin ◽  
Anticoagulant Function

Thrombomodulin (TM) is a single transmembrane, multidomain glycoprotein receptor for thrombin, and is best known for its role as a cofactor in a clinically important natural anticoagulant pathway. In addition to its anticoagulant function, TM has well-defined anti-inflammatory properties. Soluble TM levels increase significantly in the plasma of septic patients; however, the possible involvement of recombinant human soluble TM (rTM) transduction in the pathogenesis of lipopolysaccharide (LPS)-induced nephrotoxicity, including acute kidney injury (AKI), has remained unclear. Mice were injected intraperitoneally with 15 mg/kg LPS. rTM (3 mg/kg) or saline was administered to the animals before the 3 and 24 h LPS-injection. At 24 and 48 h, blood urea nitrogen, the inflammatory cytokines in sera and kidney, and histological findings were assessed. Cell activation and apoptosis signal was assessed by Western blot analysis. In this study using a mouse model of LPS-induced AKI, we found that rTM attenuated renal damage by reducing both cytokine and cell activation and apoptosis signals with the accumulation of CD4+ T-cells, CD11c+ cells, and F4/80+ cells via phospho c-Jun activations and Bax expression. These findings suggest that the mechanism underlying these effects of TM may be mediated by a reduction in inflammatory cytokine production in response to LPS. These molecules might thereby provide a new therapeutic strategy in the context of AKI with sepsis.

Protective mechanisms of protocatechuic acid against doxorubicin-induced nephrotoxicity in rat model

2019 ◽  
Vol 30 (4) ◽  
Author(s):  
Olorunfemi R. Molehin ◽  
Anne A. Adeyanju ◽  
Stephen A. Adefegha ◽  
Ajibade O. Oyeyemi ◽  
Kehinde A. Idowu
Keyword(s):  
Body Weight ◽  
Protocatechuic Acid ◽  
Serum Levels ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Protective Mechanisms ◽  
Malondialdehyde Content ◽  
Group 5 ◽  
Group 2 ◽  
Inducible Nitric Oxide

AbstractBackgroundDoxorubicin (DOX) induces toxicity in many tissues/organs, including the heart, kidney and so on. This study was designed to evaluate the modulatory effects of protocatechuic acid (PCA) against DOX-induced nephrotoxicity in rats. Animals were randomly grouped into five groups.MethodsGroup 1 served as the normal control (CTR). A single dose of DOX at 20 mg/kg was administered intraperitoneally (i.p.) to animals in Group 2. Groups 3 and 4 were pretreated with PCA for 5 days (doses of 10 and 20 mg/kg body weight, respectively) after which DOX was injected (PCA-10 + DOX and PCA-20 + DOX). Group 5 received PCA only at a dose of 20 mg/kg body weight (PCA-20).ResultsThe results revealed significant elevations (p < 0.05) in malondialdehyde content, expressions of inducible nitric oxide (iNOS) and cyclooxygenase-2 (COX2) in the kidney. Likewise, increased serum levels of creatinine and urea of DOX group were observed. A significant decrease (p < 0.05) in glutathione (GSH) level and antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione s- transferase (GST) activities in the kidney were observed compared with the control. Pretreatment with PCA (10 and 20 mg/kg, p.o.) for 5 days prior to the i.p. injection of DOX reduced MDA levels, modulated iNOS and COX2 activities and improved kidney function markers as well as oxidative stress parameters. Findings from the histopathology studies confirms the protective effects of PCA on DOX-induced damage on the kidney cells.ConclusionsThis study has demonstrated the anti-inflammatory and antioxidative properties of PCA, which could be part of its possible protective mechanisms against nephrotoxicity induced by DOX.

scholarly journals Selenium and rutin alone or in combination do not have stronger protective effects than their separate effects against cadmium-induced renal damage

2015 ◽  
Vol 54 (5) ◽  
pp. 896-904 ◽  
Author(s):  
Sunny O. Abarikwu ◽  
Olusegun L. Adebayo ◽  
Chiagoziem A. Otuechere ◽  
Blessing O. Iserhienrhien ◽  
Temitope A. Badejo
Keyword(s):  
Renal Damage ◽  
Protective Effects

scholarly journals Protocatechuic Acid Prevents oxLDL-Induced Apoptosis by Activating JNK/Nrf2 Survival Signals in Macrophages

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Rosaria Varì ◽  
Beatrice Scazzocchio ◽  
Carmela Santangelo ◽  
Carmelina Filesi ◽  
Fabio Galvano ◽  
...  
Keyword(s):  
Target Genes ◽  
Protocatechuic Acid ◽  
Biological Activities ◽  
Redox Homeostasis ◽  
Protective Effects ◽  
Antioxidant Defences ◽  
Antioxidant Power ◽  
Induced Apoptosis ◽  
P53 Target Genes ◽  
Survival Signals

Protocatechuic acid (PCA), one of the main metabolites of complex polyphenols, exerts numerous biological activities including antiapoptotic, anti-inflammatory, and antiatherosclerotic effects. Oxidised LDL have atherogenic properties by damaging arterial wall cells and inducing p53-dependent apoptosis in macrophages. This study was aimed at defining the molecular mechanism responsible for the protective effects of PCA against oxidative and proapoptotic damage exerted by oxLDL in J774 A.1 macrophages. We found that the presence of PCA in cells treated with oxLDL completely inhibited the p53-dependent apoptosis induced by oxLDL. PCA decreased oxLDL-induced ROS overproduction and in particular prevented the early increase of ROS. This decrease seemed to be the main signal responsible for maintaining the intracellular redox homeostasis hindering the activation of p53 induced by ROS, p38MAPK, and PKCδ. Consequently the overexpression of the proapoptotic p53-target genes such as p66Shc protein did not occur. Finally, we demonstrated that PCA induced the activation of JNK, which, in turn, determined the increase of nuclear Nrf2, leading to inhibition of the early ROS overproduction. We concluded that the antiapoptotic mechanism of PCA was most likely related to the activation of the JNK-mediated survival signals that strengthen the cellular antioxidant defences rather than to the PCA antioxidant power.

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