Protective Effect of Nitric Oxide on Liver Circulation from Ischemia Reperfusion Injury

Toshihiro, Watanabe; Kurata, Shinji; Sanuki, Takuro; Okayasu, Ichiro; Shibata, Yasuaki; Ikeda, Tôru; Ureshino, Hiroyuki; Ayuse, Takao

doi:10.3109/08941939.2015.1024357

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…It can interfere with the production of nitric oxide by l -arginine [ 43 ]. Previous studies found that the reduction of endogenous nitric oxide (NO) can lead to liver injury [ 44 ]. Our study found that this metabolite increased with the progress of S. japonicum infection, and it may aggravate liver injury by reducing the synthesis of nitric oxide in their bodies.…”

Section: Discussionmentioning

confidence: 99%

Alterations in gut microbiome and metabolite profile of patients with Schistosoma japonicum infection

Zhou,

Li,

Guo

et al. 2023

Parasites Vectors

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Background Schistosoma infection is a significant public health issue, affecting over 200 million individuals and threatening 700 million people worldwide. The species prevalent in China is Schistosoma japonicum. Recent studies showed that both gut microbiota and metabolome are closely related to schistosomiasis caused by S. japonicum, but clinical study is limited and the underlying mechanism is largely unclear. This study aimed to explore alterations as well as function of gut microbiota and metabolite profile in the patients with S. japonicum infection. Methods This study included 20 patients diagnosed with chronic schistosomiasis caused by S. japonicum, eight patients with advanced schistosomiasis caused by S. japonicum and 13 healthy volunteers. The fresh feces of these participators, clinical examination results and basic information were collected. 16S ribosomal RNA gene sequencing was used to investigate gut microbiota, while ultraperformance liquid chromatography-mass spectrometry (UHPLC-MS) was applied to explore the metabolome of patients in different stages of schistosomiasis. Results The study found that gut microbiota and metabolites were altered in patients with different stages of S. japonicum infection. Compared with healthy control group, the gut microbial diversity in patients with chronic S. japonicum infection was decreased significantly. However, the diversity of gut microbiota in patients with chronic schistosomiasis was similar to that in patients with advanced schistosomiasis. Compared with uninfected people, patients with schistosomiasis showed decreased Firmicutes and increased Proteobacteria. As disease progressed, Firmicutes was further reduced in patients with advanced S. japonicum infection, while Proteobacteria was further increased. In addition, the most altered metabolites in patients with S. japonicum infection were lipids and lipid-like molecules as well as organo-heterocyclic compounds, correlated with the clinical manifestations and disease progress of schistosomiasis caused by S. japonicum. Conclusions This study suggested that the gut microbiota and metabolome altered in patients in different stages of schistosomiasis, which was correlated with progression of schistosomiasis caused by S. japonicum. This inter-omics analysis may shed light on a better understanding of the mechanisms of the progression of S. japonicum infection and contribute to identifying new potential targets for the diagnosis and prognosis of S. japonicum infection. However, a large sample size of validation in clinic is needed, and further study is required to investigate the underlying mechanism.

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Section: Discussionmentioning

confidence: 99%

Alterations in gut microbiome and metabolite profile of patients with Schistosoma japonicum infection

Zhou,

Li,

Guo

et al. 2023

Parasites Vectors

View full text Add to dashboard Cite

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“…In response to the xenobiotic attack, the liver that was regenerating post-injury provides a model of cell proliferation to research the cause of the cell division modulation [ 42 , 43 , 44 ]. After cell loss in hepatotoxins induced tissue injury, the liver of mammals has been shown to possess the capacity to grow [ 45 , 46 ].…”

Section: Discussionmentioning

confidence: 99%

Is Glyceryl Trinitrate, a Nitric Oxide Donor Responsible for Ameliorating the Chemical-Induced Tissue Injury In Vivo?

Ahmed

Ahmed²,

Vun-Sang

et al. 2022

Molecules

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Oxidative stress induced by well-known toxins including ferric nitrilotriacetate (Fe-NTA), carbon tetrachloride (CCl4) and thioacetamide (TAA) has been attributed to causing tissue injury in the liver and kidney. In this study, the effect of glyceryl trinitrate (GTN), a donor of nitric oxide and NG-nitroarginine methyl ester (l-NAME), a nitric oxide inhibitor on TAA-induced hepatic oxidative stress, GSH and GSH-dependent enzymes, serum transaminases and tumor promotion markers such as ornithine decarboxylase (ODC) activity and [3H]-thymidine incorporation in rats were examined. The animals were divided into seven groups consisting of six healthy rats per group. The six rats were injected intraperitoneally with TAA to evaluate its toxic effect, improvement in its toxic effect if any, or worsening in its toxic effect if any, when given in combination with GTN or l-NAME. The single necrogenic dose of TAA administration caused a significant change in the levels of both hepatic and serum enzymes such as glutathione S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), γ-glutamyl transpeptidase (GGT), glucose 6-phosphate dehydrogenase (G6PD), alanine aminotransferase (AST) and aspartate aminotransferase (ALT). In addition, treatment with TAA also augmented malondialdehyde (MDA), ornithine decarboxylase (ODC) activity and [3H]-thymidine incorporation in rats liver. Concomitantly, TAA treatment depleted the levels of GSH. However, most of these changes were alleviated by the treatment of animals with GTN dose-dependently. The protective effect of GTN against TAA was also confirmed histopathologically. The present data confirmed our earlier findings with other oxidants including Fe-NTA and CCl4. The GTN showed no change whatsoever when administered alone, however when it was given along with TAA then it showed protection thereby contributing towards defending the role against oxidants-induced organ toxicity. Overall, GTN may contribute to protection against TAA-induced oxidative stress, toxicity, and proliferative response in the liver, according to our findings.

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“…On the other hand, the accumulation of intestinal toxins in the liver also increases ET levels. However, NO acts as a main antagonist of NO and is down-regulation during ischemia (Toshihiro et al 2015). ET can act on hepatic sinusoids, resulting in the stenosis of the liver sinusoid.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Analysis of Hepatic Microcirculation in Rabbits After Liver Ischemia-Reperfusion Injury Using Contrast-Enhanced Ultrasound

Zhou

et al. 2017

Ultrasound in Medicine & Biology

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Previous studies have shown that contrast-enhanced ultrasound (CEUS) can be used quantitatively to analyze microcirculation blood perfusion in hepatocellular carcinoma patients. However, limited data have described the application of CEUS in hepatic microcirculation after liver ischemic-reperfusion injury (IRI). The purpose of this study was to explore the use of CEUS quantitatively to assess liver microcirculation after liver IRI. We randomly sorted 45 New Zealand rabbits into 3 groups (15 in each). Group A was a control group in which the rabbits underwent laparotomy alone. In groups B and C, hepatic blood was blocked for 30 min. Simultaneously, rabbits in group C underwent left lateral lobe resection. After 30 min of ischemia, CEUS was conducted after 0 h, 1 h, 6 h and 24 h of reperfusion in the 3 groups. Time-intensity curves (TICs) for CEUS were constructed and quantitative parameters (maximum intensity [IMAX], rise time [RT], time to peak [TTP] and mean transit time [mTT]) were obtained. In addition, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were computed to estimate liver function before the operation and at 0 h, 1 h, 6 h and 24 h after reperfusion, respectively. Pathologic changes in the liver after reperfusion were also observed. Simultaneously, the correlations between serum transaminase and a variety of quantitative analysis parameters were analyzed. In groups B and C, the IMAX value decreased; whereas RT, TTP, mTT and serum ALT and AST levels increased significantly in comparison with those in group A after 0 h and 1 h of reperfusion. The pathology revealed that erythrocytes were destroyed and microcirculation was disturbed. Then, at 6 h of reperfusion, the IMAX continued to decrease. Additionally, the levels of RT, TTP, mTT and serum ALT and AST increased in comparison with those at 1 h of reperfusion. The pathologic analysis revealed inflammatory cell aggregation and leukocyte infiltration. After 24 h of reperfusion, the IMAX was reduced in comparison with that of the 6-h group. The levels of RT, TTP, mTT and serum ALT and serum AST were increased in comparison with that of the 6-h group. These findings were in accordance with the pathologic analysis. In addition, serum transaminase had a negative correlation with IMAX (p < 0.001) and a positive correlation with RT, TTP and mTT (all p < 0.001). So, in conclusion, the quantitative analysis of CEUS can be used to assess hepatic microcirculation after liver IRI.

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Protective Effect of Nitric Oxide on Liver Circulation from Ischemia Reperfusion Injury

Cited by 5 publications

References 36 publications

Alterations in gut microbiome and metabolite profile of patients with Schistosoma japonicum infection

Alterations in gut microbiome and metabolite profile of patients with Schistosoma japonicum infection

Is Glyceryl Trinitrate, a Nitric Oxide Donor Responsible for Ameliorating the Chemical-Induced Tissue Injury In Vivo?

Quantitative Analysis of Hepatic Microcirculation in Rabbits After Liver Ischemia-Reperfusion Injury Using Contrast-Enhanced Ultrasound

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