Effect of hydrogen-rich water on acute peritonitis of rat models

Zhang, Jingyao; Wu, Qifei; Song, Siyuan; Wan, Yong; Zhang, Ruiyao; Tai, Ming-Hui; Liu, Chang

doi:10.1016/j.intimp.2014.04.011

Cited by 44 publications

(28 citation statements)

References 43 publications

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“…Overproduction of reactive oxygen can result in not only direct organ injury but also exacerbation of the inflammatory reaction simultaneously. The release of proinflammatory cytokines and chemokines, including tumor necrosis factor- α (TNF- α ), interleukin-1 β (IL-1 β ), and interleukin-6 (IL-6), the most important cytokines mediating the inflammatory response, normally triggers beneficial host innate immune response to confine tissue damage [17]. Nowadays, the inhibition of inflammation by hydrogen makes sense.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Gao

Yang

Fan

et al. 2016

Mediators of Inflammation

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Doxorubicin (DOX) remains the most effective anticancer agent which is widely used in several adult and pediatric cancers, but its application is limited for its cardiotoxicity and hepatotoxicity. Hydrogen, as a selective antioxidant, is a promising potential therapeutic option for many diseases. In this study, we found that intraperitoneal injection of hydrogen-rich saline (H2 saline) ameliorated the mortality, cardiac dysfunction, and histopathological changes caused by DOX in rats. Meanwhile, serum brain natriuretic peptide (BNP), aspartate transaminase (AST), alanine transaminase (ALT), albumin (ALB), tissue reactive oxygen species (ROS), and malondialdehyde (MDA) levels were also attenuated after H2 saline treatment. What is more, we further demonstrated that H2 saline treatment could inhibit cardiac and hepatic inflammation and apoptosis relative proteins expressions by western blotting test. In conclusion, our results revealed a protective effect of H2 saline on DOX-induced cardiotoxicity and hepatotoxicity in rats by inhibiting inflammation and apoptosis.

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Section: Introductionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Gao

Yang

Fan

et al. 2016

Mediators of Inflammation

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“…There have been several studies focusing on the neuroprotective effects of HS in other nerve injury models, such as focal ischemia and reperfusion [53], Parkinson's disease [54], brain &p<0.05 vs. SAH group; &&p<0.01 vs. SAH group; @ p<0.05 vs. SAH+vehicle group; @@ p<0.01 vs. SAH+vehicle group stem infarct [55], intracerebral hemorrhage [56], neonatal hypoxia-ischemia [57], traumatic brain injury [58], spinal cord injury [59], et al, and numerous articles demonstrated that HSinduced beneficial effect is partially involved of NF-κB pathway [60][61][62]53]. As a well-established representative of inflammation, NF-κB has been reported to be activated after SAH [63][64][65].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuated Subarachnoid Hemorrhage-Induced Early Brain Injury in Rats by Suppressing Inflammatory Response: Possible Involvement of NF-κB Pathway and NLRP3 Inflammasome

et al. 2015

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Early brain injury (EBI), highlighted with inflammation and apoptosis, occurring within 72 h after subarachnoid hemorrhage (SAH), is associated with the prognosis of SAH. Recent studies have revealed that hydrogen-rich saline (HS) exerted multiple neuroprotective properties in many neurological diseases including SAH, involved to anti-oxidative and anti-apoptotic effect. We have previously reported that HS could attenuate neuronal apoptosis as well as vasospasm. However, the underlying mechanism of HS on inflammation in SAH-induced EBI remains unclear. In this study, we explored the influence of HS on nuclear factor-κB (NF-κB) pathway and nucleotide binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome at early stage after SAH, by injecting HS intraperitoneally to SAH rats. One hundred and twenty-nine SD rats were randomly divided into four groups: sham group, SAH group, SAH+vehicle group, and SAH+HS group. SAH model was conducted using endovascular perforation method; all rats were sacrificed at 24 h after SAH. Protein level of pIκBα, cytosolic and nuclear p65, NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1, interleukin-1β (IL-1β), and cleaved caspase-3 were measured by western blot. mRNA level of IL-1β, interleukin-6 (IL-6), tumor necrosis factor-c (TNF-α) were evaluated by RT-PCR. Cellular injury and death was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and Nissl staining, respectively. Our results showed that pIκBα, nuclear p65, NLRP3, ASC, caspase-1, IL-1β, cleaved caspase-3 proteins, as well as the mRNA of IL-1β, IL-6, and TNF-ɑ increased at 24 h after SAH, while cytosolic p65 decreased. TUNEL and Nissl staining presented severe cellular injury at 24 h post-SAH. However, after HS administration, the changes mentioned above were reversed. In conclusion, HS may inhibit inflammation in EBI and improve neurobehavioral outcome after SAH, partially via inactivation of NF-κB pathway and NLRP3 inflammasome. Graphical Abstract Schematic representation of the mechanism of HS-mediated anti-inflammatory effect in EBI after SAH. The NF-κB inflammatory pathway and NLRP3 inflammasome are involved in the anti-neuroinflammatory effect of HS post-SAH. SAH-induced oxidative stress enhances the activation of NF-κB, thus promoting the translocation of p65 subunit into nucleus and increasing the mRNA level of its downstream proinflammatory cytokines (IL-1β, IN-6, TNF-α) and NLRP3. Elevated expression of NLRP3 mRNA increases the assembly of NLRP3 inflammasome. In addition, oxidative stress after SAH stimulates the activation of NLRP3 inflammasome, therefore, promoting caspase-1 activation and the cleavage of pro-IL-1β into mature IL-1β. Finally, activation of NF-κB pathway and NLRP3 inflammasome contribute to the inflammation response and cellular injury in EBI after SAH. HS treatment reversed the detrimental effect mentioned above via inactivation of NF-κB pathway and NLRP3 inflammasome. ...

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“…In previous studies, scientists have proved that hydrogen had the ability of inhibiting the activation of NF-kB [15,16,27,28]. So, in this study we also investigated the activities of NF-kB in the lung tissues of different groups, and we found that hydrogen water consumption decreased the activity of NF-kB.…”

Section: Discussionmentioning

confidence: 72%