Hydrogen Gas Presents a Promising Therapeutic Strategy for Sepsis

Xie, Keliang; Liu, Lingling; Yu, Yonghao; Wang, Guolin

doi:10.1155/2014/807635

Cited by 62 publications

(40 citation statements)

References 95 publications

(115 reference statements)

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“…*P < .05 vs NC group by t test by regulating some pathways. [41][42][43] However, these molecules may not be the direct targets of hydrogen, and the final effects of hydrogen may be manifested through indirect actions. As a result, the specific mechanism of hydric action in cells needs further research.…”

Section: Discussionmentioning

confidence: 99%

Molecular hydrogen regulates PTEN‐AKT‐mTOR signaling via ROS to alleviate peritoneal dialysis‐related peritoneal fibrosis

Chen

Liu

et al. 2020

FASEB j.

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As a convenient, effective and economical kidney replacement therapy for end‐stage renal disease (ESRD), peritoneal dialysis is available in approximately 11% of ESRD patients worldwide. However, long‐term peritoneal dialysis treatment causes peritoneal fibrosis. In recent years, the application potential of molecular hydrogen in the biomedicine has been well recognized. Molecular hydrogen selectively scavenges cytotoxic reactive oxygen species (ROS) and acts as an antioxidant. In this experiment, a high glucose‐induced peritoneal fibrosis mouse model was successfully established by intraperitoneal injection of high glucose peritoneal dialysate, and peritoneal fibrosis mice were treated with hydrogen‐rich peritoneal dialysate. In addition, in vitro studies of high glucose‐induced peritoneal fibrosis were performed using MeT‐5A cells. In vitro and in vivo experiments show that molecular hydrogen could inhibit peritoneal fibrosis progress induced by high glucose effectively. Furthermore, it has been found that molecular hydrogen alleviate fibrosis by eliminating intracellular ROS and inhibiting the activation of the PTEN/AKT/mTOR pathway. The present data proposes that molecular hydrogen exerts the capacity of anti‐peritoneal fibrosis through the ROS/PTEN/AKT/mTOR pathway. Therefore, molecule hydrogen is a potential, safe, and effective treatment agent, with peritoneal protective property and great clinical significance.

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Section: Discussionmentioning

confidence: 99%

Molecular hydrogen regulates PTEN‐AKT‐mTOR signaling via ROS to alleviate peritoneal dialysis‐related peritoneal fibrosis

Chen

Liu

et al. 2020

FASEB j.

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“…Nowadays, H 2 has been recognized as a medical gas with promising potentials to prevent or cure a series of diseases, such as ischemia/reperfusion injury, neurodegeneration, metabolic syndrome, inflammation, mitochondrial diseases, and even cancers (11,30,31). Our researches published previously have revealed that 2% or 4% H 2 inhalation effectively improves survival rates of septic animals and relieves sepsis-related organ injuries (12,13).…”

Section: Discussionmentioning

confidence: 99%

“…Hydrogen gas can also protect against sepsis by modulating many signal pathways (14,20,30). Therefore, experiments were conducted to elucidate mechanisms by which H 2 modulated Caco-2 barrier function.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen-Rich Medium Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via Rhoa-Mdia1 Signaling in Caco-2 Cells

Yang

Wang

Sun

et al. 2016

Shock

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Gastrointestinal barrier dysfunction is associated with the severity and prognosis of sepsis. Hydrogen gas (H2) can ameliorate multiple organ damage in septic animals. Ras homolog gene family member A (RhoA) and mammalian diaphanous-related formin 1 (mDia1) are important to regulate tight junction (TJ) and adherens junction (AJ), both of which determine the integrity of the intestinal barrier. This study was aimed to investigate whether H2 could modulate lipopolysaccharide (LPS)-stimulated dysfunction of the intestinal barrier and whether RhoA-mDia1 signaling is involved. Caco-2 cells were exposed to different concentrations of LPS (1 μg/mL-1 mg/mL). The permeability of the intestinal barrier was evaluated by transepithelial resistance (TER) and fluorescein-isothiocyanate-dextran flux. Expression and distribution of occludin and E-cadherin were analyzed by Western blot and immunofluorescence. RhoA activity was measured by G-Lisa assay, and mDia1 expression was assessed by Western blot. LPS (100 μg/mL) decreased TER and increased fluorescein-isothiocyanate-dextran flux, which were alleviated by H2-rich medium. Also, H2 down-regulated LPS-induced oxidative stress. Moreover, H2 improved the down-regulated expression and redistribution of occludin and E-cadherin caused by LPS. Additionally, H2 alleviated LPS-caused RhoA activation, and the beneficial effects of H2 on barrier were counteracted by RhoA agonist CN03. Rho inhibitor C3 exoenzyme mitigated LPS-induced barrier breakdown. Furthermore, H2-rich medium increased mDia1 expression, and mDia1 knockdown abolished protections of H2 on barrier permeability. mDia1 knockdown eliminated H2-induced benefits for occludin and E-cadherin. These findings suggest that H2 improves LPS-induced hyperpermeability of the intestinal barrier and disruptions of TJ and AJ by moderating RhoA-mDia1 signaling.

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“…Moreover, vitamin C produces ingredients with strong oxidative power after redox reactions, leads to further DNA damage (35). Recent studies showed that H2 and/or HRSS have an effective therapeutic role in various conditions such as, organ transplantation, stroke, sepsis, multiple organ disorder syndrome, metabolic syndrome, atherosclerosis, neurodegenerative diseases and I/R injury in various organs (3,16,59,60).…”

Section: Discussionmentioning

confidence: 99%

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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Hydrogen Gas Presents a Promising Therapeutic Strategy for Sepsis

Cited by 62 publications

References 95 publications

Molecular hydrogen regulates PTEN‐AKT‐mTOR signaling via ROS to alleviate peritoneal dialysis‐related peritoneal fibrosis

Molecular hydrogen regulates PTEN‐AKT‐mTOR signaling via ROS to alleviate peritoneal dialysis‐related peritoneal fibrosis

Hydrogen-Rich Medium Ameliorates Lipopolysaccharide-Induced Barrier Dysfunction via Rhoa-Mdia1 Signaling in Caco-2 Cells

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

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