Protective effect and mechanism of hydrogen treatment on lung epithelial barrier dysfunction in rats with sepsis

Ld, Liu; Xy, Wu; Bd, Tao; N, Wang; Zhang, J

doi:10.4238/gmr.15016050

Cited by 18 publications

(14 citation statements)

References 19 publications

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“…Considering the high mortality of endotoxemia, in order to determine the best time for hydrogen treatment, we referred to the previous literature (22)(23)(24)(25) and firstly observed the 7day survival rate of animals. Thirty-three mice were randomly selected from the hydrogen treatment group and divided into three groups: hydrogen treatment after 30 min of LPS (n = 11), hydrogen treatment after 6 h of LPS (n = 11) and hydrogen treatment after 12 h of LPS (n = 11).…”

Section: Animals and Treatmentsmentioning

confidence: 99%

Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression

et al. 2021

Front. Immunol.

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Endotoxin-induced lung injury is one of the major causes of death induced by endotoxemia, however, few effective therapeutic options exist. Hydrogen inhalation has recently been shown to be an effective treatment for inflammatory lung injury, but the underlying mechanism is unknown. In the current study we aim to investigate how hydrogen attenuates endotoxin-induced lung injury and provide reference values for the clinical application of hydrogen. LPS was used to establish an endotoxin-induced lung injury mouse model. The survival rate and pulmonary pathologic changes were evaluated. THP-1 and HUVECC cells were cultured in vitro. The thioredoxin 1 (Trx1) inhibitor was used to evaluate the anti-inflammatory effects of hydrogen. Hydrogen significantly improved the survival rate of mice, reduced pulmonary edema and hemorrhage, infiltration of neutrophils, and IL-6 secretion. Inhalation of hydrogen decreased tissue factor (TF) expression and MMP-9 activity, while Trx1 expression was increased in the lungs and serum of endotoxemia mice. LPS-stimulated THP-1 and HUVEC-C cells in vitro and showed that hydrogen decreases TF expression and MMP-9 activity, which were abolished by the Trx1 inhibitor, PX12. Hydrogen attenuates endotoxin-induced lung injury by decreasing TF expression and MMP-9 activity via activating Trx1. Targeting Trx1 by hydrogen may be a potential treatment for endotoxin-induced lung injury.

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Section: Animals and Treatmentsmentioning

confidence: 99%

Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression

et al. 2021

Front. Immunol.

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“…In the L15 group, the levels of SDC-1, ICAM-1 and PVPI in group Y were not significantly different compared to group N, indicating that the endothelial polysaccharide coating structure in critically ill patients was severely damaged and could not be restored by ulinastatin alone. Due to the damage of endothelial polysaccharide coating, the increase in capillary permeability, the release of inflammatory factors and the exudation of alveolar capillaries in sepsis patients, the volume of extravascular lung water (EVLW) is increased in sepsis patients [23]. PVPI can adequately reflect the permeability of pulmonary capillaries and the value of PVPI was not increased over an increased blood volume [24].…”

Section: Baseline Characteristics Of the S15 Patients In Treatment (Y) And Control Groups (N)mentioning

confidence: 99%

The Protective Effect of Ulinastatin in Severe Sepsis. A Mechanistic Approach

Zhou¹

2020

FARMACIA

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The aim of this study was to investigate the effect of ulinastatin on endothelial polysaccharide coating and mortality in patients with severe sepsis and septic shock. Twenty-nine cases of sepsis and septic shock diagnosed from June 2015 to December 2018 were included in the study. According to their time of admission, the patients were randomly divided into ulinastatin group (Y, N = 13), which was subdivided in L15 group (APACHE II (Acute physiology and chronic health evaluation II) ≥ 15) (8 cases) and in S15 group (APACHE II < 15) (5 cases), and control group (N, N = 16), subdivided in L15 group (11 cases) and S15 group (5 cases). All patients were treated in the Intensive Care Unit (ICU). The ulinastatin group (Y) received 100,000 U ulinastatin as an intravenous infusion for a period of 8 h, while the control group received routine treatment. Temperature (T), respiratory rate (RR), heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), and pulmonary vascular permeability index (PVPI) at 0 h, 24 h and 72 h after admission were determined for each patient. Moreover, the blood samples were collected in order to evaluate the white blood cell count (WBC), lactate (Lac), C-Reactive Protein (CRP), procalcitonin (PCT), intercellular adhesion molecule (ICAM-1), Syndecan-1 (SDC-1), and systemic central venous oxygen saturation (ScVO2). The results showed that the lactate levels after 72 h of treatment and the 28-day mortality rate of group Y significantly decreased compared to group N (p <0.018). In L15 subgroup, the lactate level and the 28-day mortality rate in group Y significantly decreased compared to group N (p < 0.018). In S15 subgroup, lactate level, PVPI, SDC-1 and The 28-day mortality rate significantly decreased in group Y compared to group N (p < 0.05). In conclusion, for sepsis patients with an APACHE II score ≥ 15, their structure of vascular endothelial polysaccharide coating may be affected by many factors, and the effect of ulinastatin is limited. For sepsis patients with an APACHE II score of < 15, ulinastatin may improve vascular permeability, reduce capillary leakage and improve microcirculation by protecting the structure of endothelial polysaccharide coating. In addition, ulinastatin may reduce the mortality of sepsis patients. RezumatScopul acestui studiu a fost de a investiga efectul ulinastatinei asupra endoteliului vascular, precum și asupra mortalității la pacienții cu sepsis sever și șoc septic. Au fost incluse în studiu douăzeci și nouă de cazuri cu sepsis și șoc septic diagnosticate în perioada iunie 2015 -decembrie 2018. Pacienții au fost împărțiți astfel: grupul ulinastatină (Y, N = 13), care a fost împărțit în subgrupul L15 (APACHE II (Acute physiology and chronic health evaluation II) ≥ 15) (8 cazuri) și subrupul S15 (APACHE II <15) (5 cazuri) și respectiv grupul de control (N, N = 16), împărțit la rândul său în grupul L15 (11 cazuri) și grupul S15 (5 cazuri). Grupul ulinastatină (Y) a primit 100 000 U ulinastatină ca perfuzie intravenos timp de 8 ore, în timp ce ...

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“…Many studies have investigated how molecular hydrogen alleviates the physiological barrier damage caused by sepsis, including protective effects on vascular endothelial cells30, 35, 36, epithelial cells (e.g., alveoli and gastrointestinal epithelium)9, 11, 29, 37 and intercellular junctions9, 30, 33, 38, which are characterized by decreased permeability, increased transmembrane resistance, and regulation of expression and distribution of intercellular junction- related proteins.…”

Section: Molecular Hydrogen Reduces the Physiological Barrier Dysfuncmentioning

confidence: 99%

“…Similar to vascular endothelial cells, HRS has a protective effect on epithelial cells. Studies by Zhang et al11 and Liu et al37 have demonstrated that HRS attenuates the alveolar epithelial barrier damage caused by LPS, improves alveolar gas exchange, and reduces cell damage caused by alveolar epithelial cell apoptosis and excessive autophagy. Yang et al9 and Ikeda et al29 reported that molecular hydrogen also protects the gastrointestinal epithelial barrier during sepsis.…”

Section: Molecular Hydrogen Reduces the Physiological Barrier Dysfuncmentioning

confidence: 99%

Recent Advances in Studies of Molecular Hydrogen against Sepsis

2019

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Sepsis is a syndrome comprised of a series of life-threatening organ dysfunctions caused by a maladjusted body response to infection with no effective treatment. Molecular hydrogen is a new type of antioxidant with strong free radical scavenging ability, which has been demonstrated to be effective for treating various diseases, such as infection, trauma, poisoning, organ ischemia-reperfusion, metabolic diseases, and tumors. Molecular hydrogen exerts multiple biological effects involving anti-inflammation, anti-oxidation, anti-apoptosis, anti-shock, and autophagy regulation, which may attenuate the organ and barrier damage caused by sepsis. However, the underlying molecular mechanisms remain elusive, but are likely related to the signaling pathways involved. This review focuses on the research progress and potential mechanisms of molecular hydrogen against sepsis to provide a theoretical basis for clinical treatment.

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Protective effect and mechanism of hydrogen treatment on lung epithelial barrier dysfunction in rats with sepsis

Cited by 18 publications

References 19 publications

Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression

Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression

The Protective Effect of Ulinastatin in Severe Sepsis. A Mechanistic Approach

Recent Advances in Studies of Molecular Hydrogen against Sepsis

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