The protective role of hydrogen-rich saline in experimental liver injury in mice

Sun, Hanyong; Chen, Lei; Zhou, Weiping; Hu, Liang; Li, Liang; Tu, QianQian; Chang, Yan–Xin; Liu, Qu; Sun, Xuejun; Wu, Mengchao; Wang, HongYang

doi:10.1016/j.jhep.2010.08.011

Cited by 140 publications

(106 citation statements)

References 37 publications

(40 reference statements)

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“…We did not administrated hypothermic HHRSS to the sham group. However Sun et al (48) reported no significant biochemical and histopathologic differences between the sham and sham plus HRSS groups. Also, rat models have some limitations in mimicking human biological and physiological properties.…”

Section: Discussionmentioning

confidence: 95%

Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

Golshahi

Tavasoly

Mardjanmehr

et al. 2017

Braz. J. Vet. Pathol.

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Golshahi, et al.; Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model. Braz J Vet Pathol, 2017, 10(1), 10 -21. DOI: 10.24070/bjvp.1983 AbstractThe aim of the present study was to investigate the effects of intraportal administration of hypothermic hydrogenrich saline solution (HRSS) on hepatic ischemia/reperfusion (I/R) injury. Thirty rats were divided equally into six groups; 1) sham, no I/R or transfusion, 2) I/R injury (60 minutes ischemia + 120 minutes reperfusion, 3) I/R injury + normal saline 24°C, 4) I/R injury + normal saline 4°C, 5) I/R injury + HRSS 24°C, 6) I/R injury + HRSS 4°C. In groups 3-6, 1 mg/kg normal saline (NS) and/or HRSS were administered into the vein of the left lateral and median lobes of the liver (upper the site of clumping) 10 minutes before finishing of ischemic period. The harvest time points were at 2 hours post reperfusion in all groups. Cell death, sinusoidal dilatation, congestion, hemorrhage, and neutrophil infiltration were observed in I/R group, while these histopathological changes were attenuated in the hypothermic HRSS administrated groups (P < 0.01). The level of alanine aminotransferase, aspartate aminotransferase, malondialdehyde, interleukin 6, tumor necrosis factor a, and caspase-3 were increased significantly by I/R injury and hypothermic HRSS administration reduced all these markers (P < 0.01). SOD level was low in I/R group whereas it tended to increase in the hypothermic HRSS administrated groups (P < 0.01). The present study demonstrated that hypothermic hydrogen-rich saline solution effectively protected the hepatic tissue against cellular injury and organ dysfunction through the mechanisms that decrease the effect of oxidative stress, inflammation, apoptosis and necrosis.

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Section: Discussionmentioning

confidence: 95%

Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

Golshahi

Tavasoly

Mardjanmehr

et al. 2017

Braz. J. Vet. Pathol.

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“…When the cellular levels of ROS exceed the neutralizing capabilities of cellular nonenzymatic and enzymatic antioxidants, oxidative stress occurs. ROS plays an important role in the pathogenesis of various hepatic disorders, including I/R injury [37]. Substantial evidence has suggested that the initial production of Immunohistochemical staining for p-Akt and p-p38 was performed on liver sections from rats that had undergone 60 min of ischemia followed by 120 min (magnification, ×200) (n=6).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Two Anesthetics, Propofol and Sevoflurane, on Liver Ischemia/Reperfusion Injury

Xu¹,

J²,

Wu³

et al. 2016

Cell Physiol Biochem

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Background: Propofol and sevoflurane are widely used in clinical anesthesia, and both have been reported to exert a protective effect in organ ischemia/reperfusion (IR). This study aims to investigate and compare the effects of propofol and sevoflurane on liver ischemia/reperfusion and the precise molecular mechanism. Methods and Materials: Rats were randomized into four groups: the sham group, I/R group, propofol treatment group (infused with 1% propofol at 500 µg· kg-1· min-1), and sevoflurane treatment group (infused with 3% (2 L/min) sevoflurane). The liver ischemia/reperfusion model was used to evaluate the hepatoprotective effect on ischemic injury. Liver enzyme leakage, liver cytokines and histopathological examination were used to evaluate the extent of hepatic ischemia/reperfusion injury. Oxidative stress was investigated by evaluating the levels of Malondialdehyde(MDA), Superoxide Dismutase(SOD) and NO. The terminal dexynucleotidyl transferase(TdT)-mediated dUTP nick end labeling (TUNEL) assay and western blot were applied to detect apoptosis in the ischemic liver tissue and its mechanism. Results: Both propofol and sevoflurane attenuated the extent of hepatic ischemia/reperfusion injury which is evident from the hisopathological studies and alterations in liver enzymes such as AST and LDH by inhibiting Nuclear factor kappa B (NFκB) activation and subsequent alterations in inflammatory cytokines interleukin-1(IL-1), interleukin-6(IL-6), tumor necrosis factor-alpha (TNF-a) and increased IL10 release. Propofol exhibited a similar protective effect and a lower IL-1 release, while sevoflurane decreased TNF-a leakage more significantly. Meanwhile, oxidative stress was attenuated by reduced MDA and NO and elevated SOD release. The expression of antiapoptotic protein Bcl-2 and Bcl-xl were enhanced while that of apoptotic protein Bax and Bak were reduced by both propofol and sevoflurane to regulate hepatic apoptosis. In addition, propofol downregulated the phosphorylation of AKT and Bad protein, while sevoflurane downregulated the phosphorylation of p38. In addition, Both the treatments had no effect on the expression of AKT, Bad and p38. Conclusion: Both propofol and sevoflurane can protect the liver from ischemia/reperfusion injury by modulating the inflammatory responses reducing oxidative stress and liver apoptosis.

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“…H 2 was reported as a new antioxidant and a selective scavenger of ·OH effective in various organs (Nagata et al, 2009;Zheng et al, 2009;Sun et al, 2011). H 2 can convert hydroxyl into water (H 2 +·OH →H 2 O+·H).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap

Zhao

Wang

Qin

et al. 2013

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.

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The protective role of hydrogen-rich saline in experimental liver injury in mice

Cited by 140 publications

References 37 publications

Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

Protective effect of intraportal infusion of hypothermic hydrogen-rich saline solution on hepatic warm ischemia/reperfusion injury in rat model

The Effects of Two Anesthetics, Propofol and Sevoflurane, on Liver Ischemia/Reperfusion Injury

Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap

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