scholarly journals Effect of Mineral-Balanced Deep-Sea Water on Kidney Function and Renal Oxidative Stress Markers in Rats Fed a High-Salt Diet

2021 ◽  
Vol 22 (24) ◽  
pp. 13415
Author(s):  
So Min Jo ◽  
Jain Nam ◽  
Soo-yeon Park ◽  
Geonhee Park ◽  
Byeong Goo Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Deep Sea ◽  
Sea Water ◽  
Sodium Intake ◽  
Expression Patterns ◽  
Kidney Injury ◽  
Sprague Dawley ◽  
Deep Sea Water ◽  
High Calcium ◽  
Kidney Health

This study investigated the effect of mineral-balanced deep-sea water (DSW) on kidney health using an animal model of kidney injury due to a high-sodium diet. High magnesium/low sodium (HMLS) and high magnesium/high calcium (HMHC) DSW samples with different mineral contents were prepared. Sprague–Dawley rats were fed an 8% sodium chloride (NaCl) diet for four weeks to induce kidney injury, and each group was supplied with purified water or mineral water. Kidney injury was observed in the NaCl group according to increased kidney injury markers and malondialdehydes, providing evidence of oxidative stress. However, the kidney injury was repaired by the intake of mineral-balanced DSW. It was confirmed that the HMLS and HMHC groups showed improved Na+ excretion through the urine. Kidney injury markers in urine decreased and upregulation of low-density lipoprotein receptor-related protein2 mRNA expression was observed in the HMLS and HMHC groups. In addition, superoxide dismutase activity was increased in the HMHC groups. The gene expression patterns of the RNA sequencing were similar between the CON and HMLS groups. These results suggest that DSW has beneficial effects on kidney health due to the balanced magnesium and calcium levels in models of kidney injury caused by excessive sodium intake.

scholarly journals Anti-Inflammatory Properties of Mineral-Balanced Deep Sea Water in In-Vitro and In-Vivo Models of Inflamed Intestinal Epithelium

2020 ◽  
Vol 10 (15) ◽  
pp. 5183
Author(s):  
Jain Nam ◽  
Kyeong Jin Kim ◽  
Geonhee Park ◽  
Byeong Goo Kim ◽  
Gwi-Hwa Jeong ◽  
...  
Keyword(s):  
Deep Sea ◽  
Sea Water ◽  
Cell Model ◽  
Mineral Waters ◽  
In Vivo Models ◽  
Deep Sea Water ◽  
High Calcium ◽  
A Cell

This study aimed to determine the effect of deep-sea water (DSW)-derived mineral waters on intestinal health, using a cell model and a dextran sulfate sodium (DSS)-induced enteritis mouse model. DSW was desalted and minerals were added to generate mineral waters that were classified as trace mineral (TM), high magnesium (HM), high magnesium low salt (HMLS), and high magnesium high calcium (HMHC), using a tabletop electrodialysis device. Caco-2 cells cocultured with Raw264.7 cells were either pre-treated or not with the four water groups, and inflammation was induced by treatment with lipopolysaccharide (LPS). Compared to LPS-treated Caco-2 cells, HMLS-cotreated cells maintained high transepithelial electrical resistance, similar to control cells. FITC-dextran permeability was lower in HMLS-treated than in other cells. In vivo, in comparison to DSS-treated mice, colon shortening was inhibited, and disease activity and colon injury were suppressed in HMLS-cotreated mice. RNA-seq of colonic tissues revealed that inflammatory gene expression was similar among the control and HMLS mice, and DSS-induced expression of inflammation-related genes such as TNF-α and NOS2 and inflammatory chemokine genes was suppressed. Our findings suggest that DSW-derived mineral water intake can help reduce colitis symptoms, and the effects may be partially regulated by magnesium and other minerals.

scholarly journals Deep sea water improves exercise and inhibits oxidative stress in a physical fatigue mouse model

2016 ◽  
Vol 4 (6) ◽  
pp. 751-757 ◽  
Author(s):  
HUIJIE FAN ◽  
ZHANGBIN TAN ◽  
YUE HUA ◽  
XIAOFANG HUANG ◽  
YITING GAO ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Deep Sea ◽  
Sea Water ◽  
Physical Fatigue ◽  
Deep Sea Water

scholarly journals Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Lipid Lowering ◽  
Control Group ◽  
Sprague Dawley ◽  
Atorvastatin Group ◽  
New Strategy ◽  
Ameliorative Effect ◽  
Markers Of Oxidative Stress

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.

scholarly journals Recurrent insulin-induced hypoglycemia induces AngII and COX2 leading to renal (pro)renin receptor expression and oxidative stress

2017 ◽  
Vol 5 (1) ◽  
pp. 71 ◽  
Author(s):  
Wael Alanazi ◽  
Mohammad Uddin ◽  
Selim Fakhruddin ◽  
Keith Jackson
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Kidney Injury ◽  
Organ Damage ◽  
Day Surgery ◽  
Receptor Expression ◽  
Sprague Dawley ◽  
Subunit Expression ◽  
Renal Biomarker ◽  
And Oxidative Stress

Background: Recurrent insulin-induced hypoglycemia (RIIH) is an avoidable consequence in the therapeutic management of diabetes mellitus. RIIH has been implicated in causing hypertension through an increase in renal and systemic AngII production.Objective: The present study was performed to assess the hypothesis that chronic insulin treatment enhances AngII and COX2 formation which in turn increases (pro) renin receptor (PRR) expression and NADPH oxidase-mediated oxidative stress, leading to renal and cardiac injury.Methods: The present studies were conducted in Male Sprague Dawley rats treated with daily subcutaneous injections of 7u/kg insulin or saline for 14 days. On the 14th day, surgery was performed for treatment infusion (captopril 12mg/kg, NS398 0.3mg/kg or vehicle), and renal interstitial fluid sample and urine collections for biomarker measurements. At the end of the experiments, kidneys and hearts were harvested to evaluate PRR and NOX2 (NADPH oxidase subunit) expression and oxidative stress.Results: We found that RIIH enhanced AngII and COX2 activity, leading to renal PRR expression and NADPH oxidase-induced oxidative stress in the heart and kidney. 8-isoprostane was evaluated as a renal biomarker of oxidative stress, which was induced in insulin treated animals and modulated by captopril and NS398. In addition, there was a slight increase in NGAL, a urinary biomarker of acute kidney injury (AKI), in insulin treated animals when compared to control.Conclusion: These results demonstrate that RIIH induces renal PRR expression and oxidative stress through increasing AngII and COX2 in the heart and kidney, leading to end-organ damage.

scholarly journals Enteral Baicalin, a Flavone Glycoside, Reduces Indicators of Cardiac Surgery-Associated Acute Kidney Injury in Rats

2018 ◽  
Vol 9 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Jing Shi ◽  
Guofeng Wu ◽  
Xiaohua Zou ◽  
Ke Jiang
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Cardiac Surgery ◽  
Kidney Injury ◽  
Renal Tissue ◽  
Myeloperoxidase Activity ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Injury Index ◽  
Sprague Dawley Rats

Background/Aims: Cardiac surgery-associated acute kidney injury (CSA-AKI) is one of the most common postoperative complications in intensive care medicine. Baicalin has been shown to have anti-inflammatory and antioxidant roles in various disorders. We aimed to test the protective effects of baicalin on CSA-AKI using a rat model. Methods: Sprague-Dawley rats underwent 75 min of cardiopulmonary bypass (CPB) with 45 min of cardioplegic arrest (CA) to establish the AKI model. Baicalin was administered at different doses intragastrically 1 h before CPB. The control and treated rats were subjected to the evaluation of different kidney injury index and inflammation biomarkers. Results: Baicalin significantly attenuated CPB/CA-induced AKI in rats, as evidenced by the lower levels of serum creatinine, serum NGAL, and Kim1. Baicalin remarkably inhibited oxidative stress, reflected in the decreased malondialdehyde and myeloperoxidase activity, and enhanced superoxide dismutase activity and glutathione in renal tissue. Baicalin suppressed the expression of IL-18 and iNOS, and activated the Nrf2/HO-1 pathway. Conclusion: Our data indicated that baicalin mediated CPB/CA-induced AKI by decreasing the oxidative stress and inflammation in the renal tissues, and that baicalin possesses the potential to be developed as a therapeutic tool in clinical use for CSA-AKI.

scholarly journals Pararhodobacter marinus sp. nov., isolated from deep-sea water of the Indian Ocean

2019 ◽  
Vol 69 (4) ◽  
pp. 932-936 ◽  
Author(s):  
Qiliang Lai ◽  
Xiupian Liu ◽  
Jun Yuan ◽  
Shuchen Xie ◽  
Zongze Shao
Keyword(s):  
Indian Ocean ◽  
Deep Sea ◽  
Type Species ◽  
Sea Water ◽  
Rrna Gene ◽  
Chromosomal Dna ◽  
Content Type ◽  
Deep Sea Water ◽  
Link Type ◽  
The Indian Ocean

A taxonomic study was carried out on strain CIC4N-9T, which was isolated from deep-sea water of the Indian Ocean. The bacterium was Gram-stain-negative, catalase- and oxidase-positive, rod-shaped and non-motile. Growth was observed at salinities of 0–9% and at temperatures of 4–41 °C. The isolate was able to degrade gelatin but not aesculin. Phylogenetic analysis based on 16S rRNA gene sequences indicated that strain CIC4N-9T belonged to the genus Pararhodobacter , with the highest sequence similarity to the only recognized species, Pararhodobacter aggregans D1-19T (96.9 %). The average nucleotide identity and estimated DNA–DNA hybridization values between strain CIC4N-9T and P. aggregans D1-19T were 80.4 and 23.0 %, respectively. The principal fatty acids were summed feature 8 (C18 : 1 ω7c and/or C18 : 1 ω6c), C16 : 0, C18 : 1ω7c 11-methyl, C18 : 0 and C17 : 0. The G+C content of the chromosomal DNA was 66.8 mol%. The sole respiratory quinone was determined to be Q-10. Phosphatidylcholine, phosphatidylglycerol, phosphatidylethanolamine, diphosphatidylglycerol, two unknown phospholipids, four unknown aminolipids and one unknown polar lipid were present. The combined genotypic and phenotypic data show that strain CIC4N-9T represents a novel species within the genus Pararhodobacter , for which the name Pararhodobacter marinus sp. nov. is proposed. The type strain is CIC4N-9T (=MCCC 1A01225T=KCTC 52336T).

scholarly journals ANTIOXIDANT AND ANTI-INFLAMMATORY EFFECTS OF CURCUMIN CONTRIBUTE INTO ATTENUATION OF ACUTE GENTAMICIN-INDUCED NEPHROTOXICITY IN RATS

2019 ◽  
pp. 466-468 ◽  
Author(s):  
HAYDER M AL-KURAISHY ◽  
ALI I AL-GAREEB ◽  
HUDA ABDULBAKI RASHEED
Keyword(s):  
Oxidative Stress ◽  
Serum Creatinine ◽  
Cystatin C ◽  
Kidney Injury ◽  
Specific Situation ◽  
Distilled Water ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Group 2 ◽  
Nephroprotective Effect

Objectives: Nephrotoxicity is a renal-specific situation in which the excretion of toxic metabolites is reduced due to toxic agents and drugs. Gentamicin is an antibiotic belongs to aminoglycoside group which may induce nephrotoxicity due to induction of oxidative stress. Curcumin is a component of traditional medicine with significant nephroprotective effect. Therefore, the objective of the present study was to evaluate the nephroprotective effect of curcumin on gentamicin-induced nephrotoxicity. Methods: A total of 30 male Sprague-Dawley rats were used which divided into Group 1 (n=10): Rats treated with distilled water 5 ml/kg plus normal saline 5 ml/kg for 12 days, Group 2 (n=10): Rats treated with distilled water 5 ml/kg plus gentamicin 100 mg/kg for 12 days, and Group 3 (n=10): Rats treated with curcumin 100 mg/kg plus gentamicin 100 mg/kg for 12 days. Blood urea, serum creatinine, malondialdehyde (MDA), kidney injury molecule (KIM-1), and cystatin-C were measured in both control and experimental groups. Results: Rats treated with gentamicin showed nephrotoxicity as evident by significant elevation in blood urea, serum creatinine, KIM-1, MDA, and cystatin-C sera levels. Curcumin leads to significant reduction of blood urea and serum creatinine compared to gentamicin group, p<0.05. Curcumin also reduced MDA, KIM-1, and cystatin-C sera levels significantly compared to gentamicin group, p<0.01. Conclusion: Curcumin produced significant nephroprotective effect on gentamicin-induced nephrotoxicity through modulation of oxidative stress and inflammatory biomarkers.

Sign in / Sign up

Export Citation Format

Share Document