Qiliqiangxin Protects against Renal Injury in Rat with Cardiorenal Syndrome Type I through Regulating the Inflammatory and Oxidative Stress Signaling

Complex regional pain syndrome type I (CRPS-I) is a chronic painful condition. We investigated whether manual therapy (MT), in a chronic post-ischemia pain (CPIP) model, is capable of reducing pain behavior and oxidative stress. Male Swiss mice were subjected to ischemia-reperfusion (IR) to mimic CRPS-I. Animals received ankle joint mobilization 48h after the IR procedure, and response to mechanical stimuli was evaluated. For biochemical analyses, mitochondrial function as well as oxidative stress thiobarbituric acid reactive substances (TBARS), protein carbonyls, antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were determined. IR induced mechanical hyperalgesia which was subsequently reduced by acute MT treatment. The concentrations of oxidative stress parameters were increased following IR with MT treatment preventing these increases in malondialdehyde (MDA) and carbonyls protein. IR diminished the levels of SOD and CAT activity and MT treatment prevented this decrease in CAT but not in SOD activity. IR also diminished mitochondrial complex activity, and MT treatment was ineffective in preventing this decrease. In conclusion, repeated sessions of MT resulted in antihyperalgesic effects mediated, at least partially, through the prevention of an increase of MDA and protein carbonyls levels and an improvement in the antioxidant defense system.

Download Full-text

Levels of Proinflammatory Cytokines, Oxidative Stress, and Tissue Damage Markers in Patients with Acute Heart Failure with and without Cardiorenal Syndrome Type 1

Cardiorenal Medicine ◽

10.1159/000492602 ◽

2018 ◽

Vol 8 (4) ◽

pp. 321-331 ◽

Cited By ~ 9

Author(s):

Grazia Maria Virzì ◽

Andrea Breglia ◽

Alessandra Brocca ◽

Massimo de Cal ◽

Chiara Bolin ◽

...

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Proinflammatory Cytokines ◽

Tissue Damage ◽

Cardiorenal Syndrome ◽

Syndrome Type ◽

Spearman's Rho ◽

Spearman’S Rho ◽

And Oxidative Stress

Background: Cardiorenal syndrome type 1 (CRS type 1) is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Inflammation and oxidative stress seem to play a pivotal role in its pathophysiology. In this in vivo study, we examined the putative role of inflammation and humoral markers in the pathogenesis of the CRS type 1. Methods: We enrolled 53 patients with acute heart failure (AHF); 17 of them developed AKI (CRS type 1). The cause of AKI was presumed to be related to cardiac dysfunction after having excluded other causes. We assessed the plasma levels of proinflammatory cytokines (TNF-α, IL-6, IL-18, sICAM, RANTES, GMCSF), oxidative stress marker (myeloperoxidase, MPO), brain natriuretic peptide (BNP), and neutrophil gelatinase-associated lipocalin (NGAL) in AHF and CRS type 1 patients. Results: We observed a significant increase in IL-6, IL-18, and MPO levels in CRS type 1 group compared to AHF (p < 0.001). We found higher NGAL at admission in the CRS type 1 group compared to the AHF group (p = 0.008) and a positive correlation between NGAL and IL-6 (Spearman’s rho = 0.45, p = 0.003) and between IL-6 and BNP (Spearman’s rho = 0.43, p = 0.004). We observed lower hemoglobin levels in CRS type 1 patients compared to AHF patients (p < 0.05) and inverse correlation between hemoglobin and cytokines (IL-6: Spearman’s rho = –0.38, p = 0.005; IL-18: Spearman’s rho = –0.32, p = 0.02). Conclusion: Patients affected by CRS type 1 present increased levels of proinflammatory cytokines and oxidative stress markers, increased levels of tissue damage markers, and lower hemoglobin levels. All these factors may be implicated in the pathophysiology of CRS type 1 syndrome.

Download Full-text

Lipopolysaccharide in systemic circulation induces activation of inflammatory response and oxidative stress in cardiorenal syndrome type 1

Journal of Nephrology ◽

10.1007/s40620-019-00613-2 ◽

2019 ◽

Vol 32 (5) ◽

pp. 803-810 ◽

Cited By ~ 1

Author(s):

Grazia Maria Virzì ◽

Andrea Breglia ◽

Chiara Castellani ◽

Ghada Ankawi ◽

Chiara Bolin ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Cardiorenal Syndrome ◽

Systemic Circulation ◽

Syndrome Type ◽

And Oxidative Stress

Download Full-text

Sacran, a High-molecular Weight Polysaccharide Inhibits Renal Injury and Oxidative Stress in Chronic Renal Failure Model Rats

Journal of Nutritional Biology ◽

10.18314/jnb.v4i2.1380 ◽

2018 ◽

Vol 4 (2) ◽

pp. 267-275

Author(s):

Miwa Goto ◽

Daisuke Iohara ◽

Shinichiro Kaneko ◽

Taishi Higashi ◽

Keiichi Motoyama ◽

...

Keyword(s):

Oxidative Stress ◽

Treatment Group ◽

Renal Injury ◽

Subsequent Development ◽

Systemic Circulation ◽

Failure Model ◽

Similar Treatment ◽

Nitrogen Levels ◽

And Oxidative Stress ◽

Carbonaceous Adsorbent

The administration of a high-molecular polysaccharide Sacran results in a significant decrease in renal injury and oxidative stress, compared with that for the oral carbonaceous adsorbent, AST-120 (Kremezin®) or a non-treatment group in 5/6 nephrectomized rats. An oral administration of Sacran (20 mg/day) over a 4 week period resulted in a significant decrease in serum indoxyl sulfate, creatinine and urea nitrogen levels, compared with a similar treatment with AST-120 or the non-treatment group. Sacran treatment also resulted in antioxidant potential being maintained, compared with that for AST-120 or the non-treatment group. Immuno-histochemical analyses also demonstrated that CRF rats, when treated with Sacran, showed a decrease in the level of accumulated renal fibrosis and 8-OHdG compared with AST-120 or the non-treatment group. These results suggest that the ingestion of Sacran results in a significant reduction in the levels of prooxidants, such as uremic toxins, in the gastrointestinal tract, thereby inhibiting the subsequent development of oxidative stress in the systemic circulation.

Download Full-text

An oral absorbent, surface-deacetylated chitin nano-fiber ameliorates renal injury and oxidative stress in 5/6 nephrectomized rats

Carbohydrate Polymers ◽

10.1016/j.carbpol.2016.12.057 ◽

2017 ◽

Vol 161 ◽

pp. 21-25 ◽

Cited By ~ 14

Author(s):

Makoto Anraku ◽

Ryo Tabuchi ◽

Shinsuke Ifuku ◽

Tomone Nagae ◽

Daisuke Iohara ◽

...

Keyword(s):

Oxidative Stress ◽

Renal Injury ◽

Nano Fiber ◽

And Oxidative Stress

Download Full-text

Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis

Oxidative Medicine and Cellular Longevity ◽

10.1155/2015/391790 ◽

2015 ◽

Vol 2015 ◽

pp. 1-9 ◽

Cited By ~ 29

Author(s):

Grazia Maria Virzì ◽

Anna Clementi ◽

Massimo de Cal ◽

Alessandra Brocca ◽

Sonya Day ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Injury ◽

Cardiorenal Syndrome ◽

Syndrome Type ◽

Copper Zinc Superoxide Dismutase ◽

Stress Markers ◽

Oxidative Stress Pathway ◽

Significant Augmentation ◽

Copper Zinc

Cardiorenal Syndrome Type 1 (Type 1) is a specific condition which is characterized by a rapid worsening of cardiac function leading to acute kidney injury (AKI). Even though its pathophysiology is complex and not still completely understood, oxidative stress seems to play a pivotal role. In this study, we examined the putative role of oxidative stress in the pathogenesis of CRS Type 1. Twenty-three patients with acute heart failure (AHF) were included in the study. Subsequently, 11 patients who developed AKI due to AHF were classified as CRS Type 1. Quantitative determinations for IL-6, myeloperoxidase (MPO), nitric oxide (NO), copper/zinc superoxide dismutase (Cu/ZnSOD), and endogenous peroxidase activity (EPA) were performed. CRS Type 1 patients displayed significant augmentation in circulating ROS and RNS, as well as expression of IL-6. Quantitative analysis of all oxidative stress markers showed significantly lower oxidative stress levels in controls and AHF compared to CRS Type 1 patients (P<0.05). This pilot study demonstrates the significantly heightened presence of dual oxidative stress pathway induction in CRS Type 1 compared to AHF patients. Our findings indicate that oxidative stress is a potential therapeutic target, as it promotes inflammation by ROS/RNS-linked pathogenesis.

Download Full-text

Abstract 1476: Angiotensin II Induced Hypertrophic Response And Oxidative Stress Is Attenuated In Mice Lacking The Gene For Tnf-α

Circulation ◽

10.1161/circ.116.suppl_16.ii_304-b ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Srinivas Sriramula ◽

Nithya Mariappan ◽

Elizabeth McILwain ◽

Joseph Francis

Keyword(s):

Oxidative Stress ◽

Angiotensin Ii ◽

Cardiac Hypertrophy ◽

Collagen Type ◽

Resonance Spectroscopy ◽

Type I ◽

Ang Ii ◽

Hypertrophic Response ◽

Tnf Α ◽

And Oxidative Stress

Tumor necrosis factor-alpha (TNF-α) and angiotensin II (Ang II) play an important role in the pathophysiology of cardiovascular disease in part by inducing the cardiac hypertrophic response and oxidative stress. Recently we demonstrated that angiotensin induced hypertensive response is attenuated in mice lacking the gene for TNF-α. In this study, we examined whether Ang II induced cardiac hypertrophy and increased oxidative stress is mediated through TNF-α. Methods and results: Male TNF-α (−/−) and age matched control (WT) mice were subcutaneously implanted with osmotic minipumps containing Ang II (1 μg/kg/min) or saline for 14 days. Human recombinant TNF-α was injected in one group of TNF-α (−/−) mice (10 μg/kg/day) for 14 days. In WT+Ang mice, a temporal increase in blood pressure was observed during the study as measured by radio telemetry transmitters. At the end of the study, echocardiography revealed an increase in thickness and dimensions of left ventricle (LV) and decreased fractional shortening (%FS) in WT+Ang mice. Real time RT-PCR showed that Ang II- infusion resulted in an increase in heart/bodyweight ratio and of cardiac hypertrophy markers ANP and BNP, and profibrotic genes Collagen Type I, Collagen Type II, and TGF-β in WT mice. Electron Spin resonance spectroscopy revealed an increase in total ROS, superoxide and peroxynitrite in the WT+ANG mice when compared to control WT mice. However, these changes were all attenuated in TNF-α (−/−)+Ang mice. Ang II infusion also increased significantly the mRNA expression of gp91Phox, NOX-1, NOX-4 and AT1R in the LV of WT mice, but not in TNF-α (−/−) mice. Interestingly, injection of TNF-α in the TNF-α (−/−) mice, treated with Ang II resulted in increased cardiac hypertrophy and oxidative stress. Conclusions: Findings from the present study suggest that TNF-α plays an important role in the development of cardiac hypertrophy and oxidative stress in Ang II-induced hypertension.

Download Full-text

Abstract 371: DPPIV Inhibitor MK0626 Prevents Western Diet Induced Renal Injury via Suppression of Kidney Tissue Ras

Hypertension ◽

10.1161/hyp.62.suppl_1.a371 ◽

2013 ◽

Vol 62 (suppl_1) ◽

Author(s):

Ravi Nistala ◽

Javad Habibi ◽

Annayya Aroor ◽

Melvin R Hayden ◽

Mona Garro ◽

...

Keyword(s):

Oxidative Stress ◽

Uric Acid ◽

Renal Injury ◽

Sodium Excretion ◽

The United States ◽

Western Diet ◽

Ang Ii ◽

High Fructose ◽

Dppiv Inhibitor ◽

And Oxidative Stress

Objectives: Obesity is an independent risk factor for development and progression of renal injury. High fructose corn syrup consumption has coincided with the obesity epidemic in the United States. High fructose (60%) diets have been demonstrated to be associated with elevation in BP and worsening insulin resistance along with renal injury via increased hepatic production of uric acid. Recently, DPPIV inhibitors have been shown to improve diabetic changes and sodium excretion, effects that are beyond glycemic control. Therefore, the renal protective benefits of DPPIV inhibition in a clinically relevant Western diet fed mouse model were examined. Methods: Mice fed a high fat/high fructose (WD) diet for 16 weeks and given a DPPIV inhibitor MK0626 in their diet were examined for metabolic parameters, inflammation, kidney renin-angiotensin system (RAS) and oxidative stress. Renal injury was assessed by biochemical, immunohistological and electron microscopy techniques. In vitro , angiotensin II (Ang II) effects on OKP-PTCs were assessed for mechanism. Results: MK0626 ameliorated WD-induced increases in serum uric acid, oxidative stress and RAS. WD induced suppression of IL-10 was reversed by MK0626. There was a tendency to improve HOMA-IR by MK0626 but no effect on BP and body weights. Diet induced DPPIV activation in the plasma and kidney of WD mice was abrogated by MK0626 (~80%). WD mice were characterized by increased proteinuria (~3-fold), mesangial expansion and podocyte effacement and these changes were prevented by MK0626. In addition, the PTC endocytosis protein megalin and basilar canalicular network and mitochondrial ultrastructure abnormalities were reversed by MK0626. WD mice had decreased sodium excretion which was improved by MK0626. Ang II directly increased DPPIV activity and sodium hydrogen exchanger activity in PTCs and decreased megalin protein, which was effectively prevented by MK0626. Conclusion: Thus, WD induced increases in DPPIV activity is associated with elevations in uric acid, renal RAS, inflammation and oxidative stress which may result in renal injury. These results suggest that DPPIV inhibitors prevent WD induced renal injury and offer a novel therapy for diabetic and obesity associated renal disease.

Download Full-text

Hydrogen Gas Alleviates Chronic Intermittent Hypoxia-Induced Renal Injury through Reducing Iron Overload

Molecules ◽

10.3390/molecules24061184 ◽

2019 ◽

Vol 24 (6) ◽

pp. 1184 ◽

Cited By ~ 3

Author(s):

Peng Guan ◽

Zhi-Min Sun ◽

Li-Fei Luo ◽

Ya-Shuo Zhao ◽

Sheng-Chang Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Iron Overload ◽

Renal Injury ◽

Intermittent Hypoxia ◽

Hydrogen Gas ◽

Chronic Intermittent Hypoxia ◽

Protective Effects ◽

Divalent Metal Transporter 1 ◽

Divalent Metal Transporter ◽

And Oxidative Stress

Iron-induced oxidative stress has been found to be a central player in the pathogenesis of kidney injury. Recent studies have indicated H2 can be used as a novel antioxidant to protect cells. The present study was designed to investigate the protective effects of H2 against chronic intermittent hypoxia (CIH)-induced renal injury and its correlation mechanism involved in iron metabolism. We found that CIH-induced renal iron overloaded along with increased apoptosis and oxidative stress. Iron accumulates mainly occurred in the proximal tubule epithelial cells of rats as showed by Perl’s stain. Moreover, we found that CIH could promote renal transferrin receptor and divalent metal transporter-1 expression, inhibit ceruloplasmin expression. Renal injury, apoptosis and oxidative stress induced by CIH were strikingly attenuated in H2 treated rats. In conclusion, hydrogen may attenuate CIH-induced renal injury at least partially via inhibiting renal iron overload.

Download Full-text