Erratum: A high-salt diet enhances leukocyte adhesion in association with kidney injury in young Dahl salt-sensitive rats

Background. The study was designed to investigate if H2S could inhibit high-salt diet-induced renal excessive oxidative stress and kidney injury in Dahl rats.Methods. Male salt-sensitive Dahl and SD rats were used. Blood pressure (BP), serum creatinine, urea, creatinine clearance rate, and 24-hour urine protein were measured. Renal ultra- and microstructures were observed. Collagen-I and -III contents the oxidants and antioxidants levels in renal tissue were detected. Keap1/Nrf2 association and Keap1 s-sulfhydration were detected.Results. After 8 weeks of high-salt diet, BP was significantly increased, renal function and structure were impaired, and collagen deposition was abundant in renal tissues with increased renal MPO activity, H2O2, MDA, GSSG, and•OH contents, reduced renal T-AOC and GSH contents, CAT, GSH-PX and SOD activity, and SOD expressions in Dahl rats. Furthermore, endogenous H2S in renal tissues was decreased in Dahl rats. H2S donor, however, decreased BP, improved renal function and structure, and inhibited collagen excessive deposition in kidney, in association with increased antioxidative activity and reduced oxidative stress in renal tissues. H2S activated Nrf2 by inducing Keap1 s-sulfhydration and subsequent Keap1/Nrf2 disassociation.Conclusions. H2S protected against high-salt diet-induced renal injury associated with enhanced antioxidant capacity and inhibited renal oxidative stress.

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A high-salt diet enhances leukocyte adhesion in association with kidney injury in young dahl salt-sensitive rats

Hypertension Research ◽

10.1038/hr.2017.31 ◽

2017 ◽

Vol 40 (11) ◽

pp. 912-920 ◽

Cited By ~ 7

Author(s):

Hidenori Takahashi ◽

Suguru Nakagawa ◽

Yaqiong Wu ◽

Yukari Kawabata ◽

Atsushi Numabe ◽

...

Keyword(s):

Genetic Model ◽

Leukocyte Adhesion ◽

Kidney Damage ◽

High Salt ◽

Intercellular Adhesion Molecule ◽

Intercellular Adhesion Molecule 1 ◽

High Salt Diet ◽

Salt Loading ◽

Blood Pressure Elevation ◽

Salt Diet

Abstract Salt-sensitive hypertension is associated with severe organ damage. Generating oxygen radicals is an integral component of salt-induced kidney damage, and activated leukocytes are important in oxygen radical biosynthesis. We hypothesized that a high-salt diet causes the upregulation of immune-related mechanisms, thereby contributing to the susceptibility of Dahl salt-sensitive rats to hypertensive kidney damage. For verifying the hypothesis, we investigated leukocytes adhering to retinal vessels when Dahl salt-sensitive rats were challenged with a high-salt (8% NaCl) diet using acridine orange fluoroscopy and a scanning laser ophthalmoscope. The high-salt diet increased leukocyte adhesion after 3 days and was associated with a significant increase in mRNA biosynthesis of monocyte chemotactic protein-1 and intercellular adhesion molecule-1 (ICAM-1) -related molecules in the kidney. Losartan treatment did not affect increased leukocyte adhesion during the early, pre-hypertensive phase of high salt loading; however, losartan attenuated the adhesion of leukocytes during the hypertensive stage. Moreover, the inhibition of leukocyte adhesion in the pre-hypertensive stage by anti-CD18 antibodies decreased tethering of leukocytes and was associated with the attenuation of functional and morphological kidney damage without affecting blood pressure elevation. In conclusion, a high-salt challenge rapidly increased leukocyte adhesion through the over-expression of ICAM-1. Increased leukocyte adhesion in the pre-hypertensive stage is responsible for subsequent kidney damage in Dahl salt-sensitive rats. Immune system involvement may be a key component that initiates kidney damage in a genetic model of salt-induced hypertension.

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Serum Untargeted Metabolism Reveals the Mechanism of L. plantarum ZDY2013 in Alleviating Kidney Injury Induced by High-Salt Diet

Nutrients ◽

10.3390/nu13113920 ◽

2021 ◽

Vol 13 (11) ◽

pp. 3920

Author(s):

Cuixiang Wan ◽

Shufang Chen ◽

Kui Zhao ◽

Zhongyue Ren ◽

Lingling Peng ◽

...

Keyword(s):

Renal Injury ◽

Intestinal Inflammation ◽

Intestinal Flora ◽

Kidney Injury ◽

High Salt ◽

Uremic Toxins ◽

Rrna Gene ◽

Mice Model ◽

High Salt Diet ◽

Salt Diet

A high-salt diet (HSD) is one of the key risk factors for hypertension and kidney injury. In this study, a HSD C57BL/6J mice model was established with 4% NaCl, and then different concentrations of Lactobacillus plantarum ZDY2013 were intragastrically administered for 2 weeks to alleviate HSD-induced renal injury. For the study, 16S rRNA gene sequencing, non-targeted metabonomics, real-time fluorescent quantitative PCR, and Masson’s staining were used to investigate the mechanism of L. plantarum ZDY2013 in alleviating renal damage. Results showed that HSD caused intestinal inflammation and changed the intestinal permeability of mice, disrupted the balance of intestinal flora, and increased toxic metabolites (tetrahydrocorticosteron (THB), 3-methyhistidine (3-MH), creatinine, urea, and L-kynurenine), resulting in serious kidney damage. Interestingly, L. plantarum ZDY2013 contributed to reconstructing the intestinal flora of mice by increasing the level of Lactobacillus and Bifidobacterium and decreasing that of Prevotella and Bacteroides. Moreover, the reconstructed intestinal microbiota significantly changed the concentration of the metabolites of hosts through metabolic pathways, including TCA cycle, ABC transport, purine metabolism, and histidine metabolism. The content of uremic toxins such as L-kynurenine, creatinine, and urea in the serum of mice was found to be decreased by L. plantarum ZDY2013, which resulted in renal injury alleviation. Our data suggest that L. plantarum ZDY2013 can indeed improve chronic kidney injury by regulating intestinal flora, strengthening the intestinal barrier, limiting inflammatory response, and reducing uremic toxins.

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Implantation and pregnancy outcome of rats fed with low and high salt diet

Endocrine Abstracts ◽

10.1530/endoabs.38.p361 ◽

2015 ◽

Author(s):

Iranloye Bolanle ◽

Oludare Gabriel

Keyword(s):

Pregnancy Outcome ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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463-P: Deterioration of Atherosclerosis via Dysbiosis in ApoE Null Mice Fed with High-Salt Diet

Diabetes ◽

10.2337/db20-463-p ◽

2020 ◽

Vol 69 (Supplement 1) ◽

pp. 463-P

Author(s):

TOMONORI KIMURA ◽

YOSHITAKA HASHIMOTO ◽

TAKAFUMI SENMARU ◽

EMI USHIGOME ◽

MASAHIDE HAMAGUCHI ◽

...

Keyword(s):

High Salt ◽

High Salt Diet ◽

Salt Diet

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Faculty Opinions recommendation of ET-1 increases reactive oxygen species following hypoxia and high-salt diet in the mouse glomerulus.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.718876812.793503540 ◽

2015 ◽

Author(s):

Fredrik Palm

Keyword(s):

Reactive Oxygen Species ◽

Reactive Oxygen ◽

High Salt ◽

Oxygen Species ◽

High Salt Diet ◽

Salt Diet

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Metabolic Syndrome and Salt-Sensitive Hypertension in Polygenic Obese TALLYHO/JngJ Mice: Role of Na/K-ATPase Signaling

International Journal of Molecular Sciences ◽

10.3390/ijms20143495 ◽

2019 ◽

Vol 20 (14) ◽

pp. 3495 ◽

Cited By ~ 1

Author(s):

Yanling Yan ◽

Jiayan Wang ◽

Muhammad A. Chaudhry ◽

Ying Nie ◽

Shuyan Sun ◽

...

Keyword(s):

Blood Pressure ◽

Renal Function ◽

Significant Rise ◽

Protein Carbonylation ◽

High Salt ◽

Kidney Cortex ◽

High Salt Diet ◽

Salt Diet ◽

Salt Sensitive Hypertension

We have demonstrated that Na/K-ATPase acts as a receptor for reactive oxygen species (ROS), regulating renal Na+ handling and blood pressure. TALLYHO/JngJ (TH) mice are believed to mimic the state of obesity in humans with a polygenic background of type 2 diabetes. This present work is to investigate the role of Na/K-ATPase signaling in TH mice, focusing on susceptibility to hypertension due to chronic excess salt ingestion. Age-matched male TH and the control C57BL/6J (B6) mice were fed either normal diet or high salt diet (HS: 2, 4, and 8% NaCl) to construct the renal function curve. Na/K-ATPase signaling including c-Src and ERK1/2 phosphorylation, as well as protein carbonylation (a commonly used marker for enhanced ROS production), were assessed in the kidney cortex tissues by Western blot. Urinary and plasma Na+ levels were measured by flame photometry. When compared to B6 mice, TH mice developed salt-sensitive hypertension and responded to a high salt diet with a significant rise in systolic blood pressure indicative of a blunted pressure-natriuresis relationship. These findings were evidenced by a decrease in total and fractional Na+ excretion and a right-shifted renal function curve with a reduced slope. This salt-sensitive hypertension correlated with changes in the Na/K-ATPase signaling. Specifically, Na/K-ATPase signaling was not able to be stimulated by HS due to the activated baseline protein carbonylation, phosphorylation of c-Src and ERK1/2. These findings support the emerging view that Na/K-ATPase signaling contributes to metabolic disease and suggest that malfunction of the Na/K-ATPase signaling may promote the development of salt-sensitive hypertension in obesity. The increased basal level of renal Na/K-ATPase-dependent redox signaling may be responsible for the development of salt-sensitive hypertension in polygenic obese TH mice.

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