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

Nutrients ◽  
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.

Abstract 16835: Targeted Disruption of Paraoxonase 3 in a Dahl Salt-Sensitive Rat Model of Chronic Kidney Disease Increases Renal Cortical Pro-Inflammatory Eicosanoids

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Chrysan J Mohammed ◽  
Fatimah K Khalaf ◽  
Prabhatchandra Dube ◽  
Tyler J Reid ◽  
Jacob A Connolly ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Renal Cortex ◽  
High Salt ◽  
High Density Lipoproteins ◽  
Wild Type ◽  
Targeted Disruption ◽  
High Salt Diet ◽  
Salt Diet ◽  
Mediators Of Inflammation

Background: Paraoxonase 3 (Pon3), is one of the three isoforms of the paraoxonase gene family. While Pon1 and Pon2 are widely studied, there is a paucity of knowledge regarding Pon3. Pon3 is synthesized in the liver and can circulate bound to high-density lipoproteins. There is significant expression in the kidney also. Pon3 has the ability to metabolize eicosanoids, which can act as signaling molecules and have known roles in the pathophysiology of some renal diseases. Decreased Pon activity is associated with elevated levels of eicosanoid metabolites and adverse clinical outcomes. We tested the hypothesis that targeted disruption of Pon3 results in elevated levels of pro-inflammatory eicosanoids and progression of renal injury. Methods/ Results: Ten week old male Dahl salt-sensitive (SS rats) and Pon3 mutant rats (SS Pon3 KO) were maintained on 8% high salt diet for eight weeks, to initiate salt-sensitive hypertensive renal disease. Previously we observed that SS Pon3 KO rats on eight weeks high salt diet demonstrated significantly increased phenotypic renal injury and mortality. In the current study, we noted that SS Pon3 KO had significantly decreased (p<0.05) glomerular filtration rate compared to SS wild type. Blood pressure (radiotelemetry) as well as plasma angiotensin and aldosterone (LC-MS/MS) were not different between the two groups after high salt diet. We used targeted lipidomic profiling to determine eicosanoid content in renal cortex from SS Pon3 KO and SS wild type rats at the end of eight weeks of high salt diet. We found that hydroxyl fatty acids 5-HEPE and 5-HETE (5-lipoxygenase dependent arachidonic acid metabolites) were significantly (p<0.05) elevated in the renal cortex of SS Pon3 KO compared to SS wild type rats. In addition to being mediators of inflammation, these metabolites are associated with renal cell injury and death. Furthermore, prostaglandin 6-keto-PGF 1α , which has known links to renal inflammation, was significantly (p<0.05) increased in renal cortex of SS- Pon3 KO compared to SS wild type rats. Conclusion: These findings suggest that targeted deletion of Pon3 increases pro-inflammatory eicosanoids (5-HETE and 5-HEPE) and prostaglandins (6-keto-PGF 1α ), as well as increases renal damage independent of blood pressure.

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

2017 ◽  
Vol 40 (11) ◽  
pp. 945-945
Author(s):  
Hidenori Takahashi ◽  
Suguru Nakagawa ◽  
Yaqiong Wu ◽  
Yukari Kawabata ◽  
Atsushi Numabe ◽  
...  
Keyword(s):  
Leukocyte Adhesion ◽  
Kidney Injury ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Association of a Disrupted Dipping Pattern of Blood Pressure with Progression of Renal Injury during the Development of Salt-Dependent Hypertension in Rats

2020 ◽  
Vol 21 (6) ◽  
pp. 2248 ◽  
Author(s):  
Abu Sufiun ◽  
Asadur Rahman ◽  
Kazi Rafiq ◽  
Yoshihide Fujisawa ◽  
Daisuke Nakano ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Circadian Rhythm ◽  
Renal Injury ◽  
Tissue Injury ◽  
Renal Tissue ◽  
High Salt ◽  
Hypertensive Rats ◽  
High Salt Diet ◽  
Salt Diet ◽  
The Difference

The aim of the present study is to investigate whether a disruption of the dipping pattern of blood pressure (BP) is associated with the progression of renal injury in Dahl salt-sensitive (DSS) hypertensive rats. Seven-week-old DSS rats were fed a high salt diet (HSD; 8% NaCl) for 10 weeks, followed by a transition to a normal salt diet (NSD; 0.3% NaCl) for 4 weeks. At baseline, NSD-fed DSS rats showed a dipper-type circadian rhythm of BP. By contrast, HSD for 5 days caused a significant increase in the difference between the active and inactive periods of BP with an extreme dipper type of BP, while proteinuria and renal tissue injury were not observed. Interestingly, HSD feeding for 10 weeks developed hypertension with a non-dipper pattern of BP, which was associated with obvious proteinuria and renal tissue injury. Four weeks after switching to an NSD, BP and proteinuria were significantly decreased, and the BP circadian rhythm returned to the normal dipper pattern. These data suggest that the non-dipper pattern of BP is associated with the progression of renal injury during the development of salt-dependent hypertension.

scholarly journals Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension

2020 ◽  
Vol 126 (7) ◽  
pp. 839-853 ◽  
Author(s):  
Xuefang Yan ◽  
Jiajia Jin ◽  
Xinhuan Su ◽  
Xianlun Yin ◽  
Jing Gao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arachidonic Acid ◽  
Fecal Microbiota Transplantation ◽  
Intestinal Flora ◽  
Corticosterone Level ◽  
Fecal Microbiota ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Induced Hypertension

Rationale: High-salt diet is one of the most important risk factors for hypertension. Intestinal flora has been reported to be associated with high salt–induced hypertension (hSIH). However, the detailed roles of intestinal flora in hSIH pathogenesis have not yet been fully elucidated. Objective: To reveal the roles and mechanisms of intestinal flora in hSIH development. Methods and Results: The abovementioned issues were investigated using various techniques including 16S rRNA gene sequencing, untargeted metabolomics, selective bacterial culture, and fecal microbiota transplantation. We found that high-salt diet induced hypertension in Wistar rats. The fecal microbiota of healthy rats could dramatically lower blood pressure (BP) of hypertensive rats, whereas the fecal microbiota of hSIH rats had opposite effects. The composition, metabolism, and interrelationship of intestinal flora in hSIH rats were considerably reshaped, including the increased corticosterone level and reduced Bacteroides and arachidonic acid levels, which tightly correlated with BP. The serum corticosterone level was also significantly increased in rats with hSIH. Furthermore, the above abnormalities were confirmed in patients with hypertension. The intestinal Bacteroides fragilis could inhibit the production of intestinal-derived corticosterone induced by high-salt diet through its metabolite arachidonic acid. Conclusions: hSIH could be transferred by fecal microbiota transplantation, indicating the pivotal roles of intestinal flora in hSIH development. High-salt diet reduced the levels of B fragilis and arachidonic acid in the intestine, which increased intestinal-derived corticosterone production and corticosterone levels in serum and intestine, thereby promoting BP elevation. This study revealed a novel mechanism different from inflammation/immunity by which intestinal flora regulated BP, namely intestinal flora could modulate BP by affecting steroid hormone levels. These findings enriched the understanding of the function of intestinal flora and its effects on hypertension.

Melatonin prevents kidney injury in a high salt diet-induced hypertension model by decreasing oxidative stress

2015 ◽  
Vol 60 (1) ◽  
pp. 48-54 ◽  
Author(s):  
Avshalom Leibowitz ◽  
Alexander Volkov ◽  
Konstantin Voloshin ◽  
Chen Shemesh ◽  
Iris Barshack ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Injury ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Induced Hypertension

Calcitriol ameliorates damage in high-salt diet-induced hypertension: Evidence of communication with the gut–kidney axis

2021 ◽  
pp. 153537022110625
Author(s):  
Ruifeng Ding ◽  
Zilong Xiao ◽  
Yufeng Jiang ◽  
Yi Yang ◽  
Yang Ji ◽  
...  
Keyword(s):  
Vitamin D ◽  
Gut Microbiota ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Vitamin D Supplementation ◽  
High Salt ◽  
Intestinal Barrier Function ◽  
High Salt Diet ◽  
Salt Diet ◽  
Induced Hypertension

Several studies have established a link between high-salt diet, inflammation, and hypertension. Vitamin D supplementation has shown anti-inflammatory effects in many diseases; gut microbiota is also associated with a wide variety of cardiovascular diseases, but potential role of vitamin D and gut microbiota in high-salt diet-induced hypertension remains unclear. Therefore, we used rats with hypertension induced by a high-salt diet as the research object and analyzed the transcriptome of their tissues (kidney and colon) and gut microbiome to conduct an overall analysis of the gut–kidney axis. We aimed to confirm the effects of high salt and calcitriol on the gut–kidney immune system and the composition of the intestinal flora. We demonstrate that consumption of a high-salt diet results in hypertension and inflammation in the colon and kidney and alteration of gut microbiota composition and function. High-salt diet-induced hypertension was found to be associated with seven microbial taxa and mainly associated with reduced production of the protective short-chain fatty acid butyrate. Calcitriol can reduce colon and kidney inflammation, and there are gene expression changes consistent with restored intestinal barrier function. The protective effect of calcitriol may be mediated indirectly by immunological properties. Additionally, the molecular pathways of the gut microbiota-mediated blood pressure regulation may be related to circadian rhythm signals, which needs to be further investigated. An innovative association analysis of the microbiota may be a key strategy to understanding the association between gene patterns and host.

The N-type and L-type calcium channel blocker cilnidipine suppresses renal injury in Dahl rats fed a high-salt diet

2010 ◽  
Vol 25 (6) ◽  
pp. 549-555 ◽  
Author(s):  
Shizuka Aritomi ◽  
Hajime Koganei ◽  
Hirotaka Wagatsuma ◽  
Akira Mitsui ◽  
Tetsuya Ogawa ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Renal Injury ◽  
Channel Blocker ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet

scholarly journals Sodium bicarbonate loading limits tubular cast formation independent of glomerular injury and proteinuria in Dahl salt-sensitive rats

2018 ◽  
Vol 132 (11) ◽  
pp. 1179-1197 ◽  
Author(s):  
Sarah C. Ray ◽  
Bansari Patel ◽  
Debra L. Irsik ◽  
Jingping Sun ◽  
Hiram Ocasio ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Bicarbonate ◽  
Renal Injury ◽  
High Salt ◽  
Proton Channel ◽  
Pathological Feature ◽  
Glomerular Injury ◽  
High Salt Diet ◽  
Salt Diet ◽  
Inflammatory Status

Sodium bicarbonate (NaHCO3) slows the decline in kidney function in patients with chronic kidney disease (CKD), yet the mechanisms mediating this effect remain unclear. The Dahl salt-sensitive (SS) rat develops hypertension and progressive renal injury when fed a high salt diet; however, the effect of alkali loading on kidney injury has never been investigated in this model. We hypothesized that NaHCO3 protects from the development of renal injury in Dahl salt-sensitive rats via luminal alkalization which limits the formation of tubular casts, which are a prominent pathological feature in this model. To examine this hypothesis, we determined blood pressure and renal injury responses in Dahl SS rats drinking vehicle (0.1 M NaCl) or NaHCO3 (0.1 M) solutions as well as in Dahl SS rats lacking the voltage-gated proton channel (Hv1). We found that oral NaHCO3 reduced tubular NH4+ production, tubular cast formation, and interstitial fibrosis in rats fed a high salt diet for 2 weeks. This effect was independent of changes in blood pressure, glomerular injury, or proteinuria and did not associate with changes in renal inflammatory status. We found that null mutation of Hv1 also limited cast formation in Dahl SS rats independent of proteinuria or glomerular injury. As Hv1 is localized to the luminal membrane of TAL, our data suggest that alkalization of the luminal fluid within this segment limits cast formation in this model. Reduced cast formation, secondary to luminal alkalization within TAL segments may mediate some of the protective effects of alkali loading observed in CKD patients.

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