Protective Effects Of Hydrogen-rich Saline Research Articles

Hydrogen-rich saline reduces tissue injury and improves skin flap survival on a rat hindlimb degloving injury model

Degloving injuries represent a challenge in plastic surgery. The aim of this study is to acknowledge the protective effects of hydrogen-rich saline (HRS) solution on a rat hindlimb degloved skin flap. Twenty-one Sprague-Dawley rats were divided into three groups (control, saline and HRS). Degloving injury model was established, and flaps were sutured back following 5min of ischemia. The control group did not receive any treatment. The saline group received intraperitoneal physiological saline (10 ml/kg) and the HRS group received intraperitoneal HRS solution (10 ml/kg) postoperatively and daily for 5 days after the operation. Skin samples were obtained for histological, immunohistochemical and biochemical evaluations. Inflammation was lower in the HRS compared with saline (p = 0.02) and control (p = 0.004) groups. Edema was lower in the HRS compared with saline (p = 0.02) and control (p = 0.001) groups. Malondialdehyde (MDA) level was lower in the HRS than the control group (p = 0.01). Total antioxidant level was higher in the HRS compared with saline (p = 0.009) and control (p = 0.03) groups. Total oxidant level was lower in the HRS than the control group (p = 0.02). Oxidative stress index was lower in the HRS compared with saline (p = 0.001) and control (p = 0.0001) groups`. Vascular proliferation was higher in the HRS compared with the control group (p = 0.01). Repeated HRS injections after trauma increased the viability of skin flap in rat degloving injury model by decreasing local tissue injury, due to its antioxidant, anti-inflammatory and angiogenic effects.

Hydrogen-Rich Saline Ameliorates Experimental Autoimmune Encephalomyelitis in C57BL/6 Mice Via the Nrf2-ARE Signaling Pathway

Multiple sclerosis (MS) is a chronic and inflammatory disease of the central nervous system that is associated with demyelination, neurodegeneration, and sensitivity to oxidative stress. Hydrogen-rich saline (HRS) is efficacious in preventive and therapeutic applications for many disorders because of its antioxidant and anti-inflammatory properties. Here, we determined the effect of HRS in experimental autoimmune encephalomyelitis (EAE), which is a generally accepted model of the immuno-pathogenic mechanisms underlying MS. We found that HRS reduced the severity of EAE in mice and alleviated inflammation and demyelination. Furthermore, treatment with HRS attenuated oxidative stress in EAE mice. Finally, the results of our study suggest that activation of the Nrf2-ARE pathway plays a critical role in the protective effects of HRS in EAE mice.

Protective Effects of Hydrogen-Rich Saline Against Lipopolysaccharide-Induced Alveolar Epithelial-to-Mesenchymal Transition and Pulmonary Fibrosis.

BackgroundFibrotic change is one of the important reasons for the poor prognosis of patients with acute respiratory distress syndrome (ARDS). The present study investigated the effects of hydrogen-rich saline, a selective hydroxyl radical scavenger, on lipopolysaccharide (LPS)-induced pulmonary fibrosis.Material/MethodsMale ICR mice were divided randomly into 5 groups: Control, LPS-treated plus vehicle treatment, and LPS-treated plus hydrogen-rich saline (2.5, 5, or 10 ml/kg) treatment. Twenty-eight days later, fibrosis was assessed by determination of collagen deposition, hydroxyproline, and type I collagen levels. Development of epithelial-to-mesenchymal transition (EMT) was identified by examining protein expressions of E-cadherin and α-smooth muscle actin (α-SMA). Transforming growth factor (TGF)-β1 content, total antioxidant capacity (T-AOC), malondialdehyde (MDA) content, catalase (CAT), and superoxide dismutase (SOD) activity were determined.ResultsMice exhibited increases in collagen deposition, hydroxyproline, type I collagen contents, and TGF-β1 production in lung tissues after LPS treatment. LPS-induced lung fibrosis was associated with increased expression of α-SMA, as well as decreased expression of E-cadherin. In addition, LPS treatment increased MDA levels but decreased T-AOC, CAT, and SOD activities in lung tissues, indicating that LPS induced pulmonary oxidative stress. Hydrogen-rich saline treatment at doses of 2.5, 5, or 10 ml/kg significantly attenuated LPS-induced pulmonary fibrosis. LPS-induced loss of E-cadherin in lung tissues was largely reversed, whereas the acquisition of α-SMA was dramatically decreased by hydrogen-rich saline treatment. In addition, hydrogen-rich saline treatment significantly attenuated LPS-induced oxidative stress.ConclusionsHydrogen-rich saline may protect against LPS-induced EMT and pulmonary fibrosis through suppressing oxidative stress.

Hydrogen-rich saline attenuates hippocampus endoplasmic reticulum stress after cardiac arrest in rats

BackgroundHydrogen-rich saline can selectively scavenge reactive oxygen species (ROS) and protect brain against ischemia reperfusion (I/R) injury. Endoplasmic reticulum stress (ERS) has been implicated in the pathological process of cerebral ischemia. However, very little is known about the role of hydrogen-rich saline in mediating pathophysiological reactions to ERS after I/R injury caused by cardiac arrest. MethodsThe rats were randomly divided into three groups, sham group (n=30), ischemia/reperfusion group (n=40) and hydrogen-rich saline group (n=40). The rats in experimental groups were subjected to 4min of cardiac arrest and followed by resuscitation. Then they were randomized to receive 5ml/kg of either hydrogen-rich saline or normal saline. ResultsHydrogen-rich saline significantly improves survival rate and neurological function. The beneficial effects of hydrogen-rich saline were associated with decreased levels of oxidative products, as well as the increased levels of antioxidant enzymes. Furthermore, the protective effects of hydrogen-rich saline were accompanied by the increased activity of glucose-regulated protein 78 (GRP78), the decreased activity of cysteinyl aspartate specific proteinase-12 (caspase-12) and C/EBP homologous protein (CHOP). ConclusionsHydrogen-rich saline attenuates brain I/R injury may through inhibiting hippocampus ERS after cardiac arrest in rats.

Protective effects of hydrogen-rich saline against N-methyl-N-nitrosourea-induced photoreceptor degeneration

The N-methyl-N-nitrosourea (MNU)-treated rat is typically used as an animal model of chemically-induced retinitis pigmentosa (RP). Reactive oxygen species (ROS) have been recognized as the crucial contributor to the retinal photoreceptor apoptosis seen in MNU-treated rats. In the present study, we explored the therapeutic effects of hydrogen-rich saline (HRS), a selective ROS scavenger, on MNU-induced photoreceptor degeneration. Intraperitoneal (IP) administration of HRS ameliorated MNU-induced photoreceptor degeneration in terms of morphology and function: Sharply decreased thickness of the retinal outer nuclear layer (ONL) and flattened photopic and scotopic electroretinogram (ERG) waveforms, typically seen in response to MNU treatment, were substantially rescued in rats cotreated with MNU and HRS (MNU + HRS). Moreover, the terminal deoxyuridine triphosphate nick-end labeling (TUNEL) assay revealed a smaller number of apoptotic photoreceptors in the MNU + HRS group compared that in the MNU group. Compared to MNU-treated rats, retinal malondialdehyde (MDA) content in MNU + HRS rats significantly decreased while superoxide dismutase (SOD) activity significantly increased. Morphological and multi-electrode array (MEA) analyses revealed more efficient preservation of the architecture and field potential waveforms in particularly the peripheral regions of the retinas within the MNU + HRS group, compared to that in the MNU group. However, this enhanced protection of structure and function in the peripheral retina is unlikely the result of site-dependent variation in the efficacy of HRS; rather, it is most likely due to reduced susceptibility of peripheral photoreceptors to MNU-induced degeneration. Inner retinal neuron function in the MNU + HRS rats was better preserved, with fewer apoptotic photoreceptors in the ONL. Collectively, these results support the rationale for future clinical evaluation of HRS as a therapeutic agent for human RP.

Protective Effects of Hydrogen-Rich Saline on Rats with Smoke Inhalation Injury.

Objective. To explore the protective effects of hydrogen-rich saline on rats with smoke inhalation injury. Methods. 36 healthy male Sprague-Dawley rats were randomly divided into 3 groups (n = 12 per group): sham group (S), inhalation injury plus normal saline treatment group (I+NS), and inhalation injury plus hydrogen-rich saline treatment group (I+HS). 30 min after injury, normal saline and hydrogen-rich saline were injected intraperitoneally (5 mL/kg) in I+NS group and I+HS group, respectively. All rats were euthanized and blood and organ specimens were collected for determination 24 h after inhalation injury. Results. Tumor necrosis factor-alpha (TNF-α) levels, malondialdehyde (MDA) concentrations, nuclear factor kappa B (NF-κB) p65 expression, and apoptosis index (AI) in I+HS group were significantly decreased (P < 0.05), while superoxide dismutase (SOD) activities were increased compared with those in I+NS group; and a marked improvement in alveolar structure was also found after hydrogen-rich saline treatment. Conclusions. Hydrogen-rich saline treatment exerts protective effects in acute lung injury induced by inhalation injury, at least in part through the activation of anti-inflammatory and antioxidant pathways and inhibition of apoptosis.

Hydrogen-rich saline protects against ischemia/reperfusion injury in grafts after pancreas transplantations by reducing oxidative stress in rats.

Purpose. This study aimed to investigate the therapeutic potential of hydrogen-rich saline on pancreatic ischemia/reperfusion (I/R) injury in rats. Methods. Eighty heterotopic pancreas transplantations (HPT) were performed in syngenic rats. The receptors were randomized blindly into the following three groups: the HPT group and two groups that underwent transplantation and administration of hydrogen-rich saline (HS, >0.6 mM, 6 mL/kg) or normal saline (NS, 6 mL/kg) via the tail vein at the beginning of reperfusion (HPT + HS group, HPT + NS group). Samples from the pancreas and blood were taken at 12 hours after reperfusion. The protective effects of hydrogen-rich saline against I/R injury were evaluated by determining the changes in histopathology and measuring serological parameters, oxidative stress-associated molecules, and proinflammatory cytokines. Results. Administration of hydrogen-rich saline produced notable protection against pancreatic I/R injury in rats. Histopathological improvements and recovery of impaired pancreatic function were observed. In addition, TNF-α, IL-1β, and IL-6 were reduced markedly in the HPT + HS group. Additionally, there were noticeable inhibitory effects on the pancreatic malondialdehyde level and considerable recruitment of SOD and GPx, which are antioxidants. Conclusion. Hydrogen-rich saline treatment significantly attenuated the severity of pancreatic I/R injury in rats, possibly by reducing oxidative stress and inflammation.

Protective effects of hydrogen-rich saline in uncontrolled hemorrhagic shock.

Hydrogen is considered to be a novel antioxidant as it inhibits inflammation, removes oxygen-derived free radicals and reduces oxidative damage. This study investigated the effects of hydrogen-rich saline on plasma interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD) and malondialdehyde (MDA) in rats with uncontrolled hemorrhagic shock (UHS). The UHS model was induced by arterial bleeding and tail amputation. The rats were randomly divided into: Group A (sham-operated group), Group B [shock + intravenously (IV) injected saline], Group C (shock + IV-injected hydrogen-rich saline), Group D [shock + intraperitoneally (IP) injected saline] and Group E (shock + IP-injected hydrogen-rich saline). The survival rate 24 h after successful resuscitation was calculated. The mean arterial pressure and heart rate were recorded at 0, 30, 90 and 210 min. The plasma levels of IL-6, TNF-α, SOD and MDA were measured at 0, 90 and 210 min. The survival rate of each group was 100% and the hemodynamics among the experimental groups were not significantly different. At 90 and 210 min, the levels of IL-6, TNF-α and MDA in Groups C and E were lower than those of Groups B and D, while the SOD levels were higher than those of Groups B and D (P<0.01). At 90 min, the levels of IL-6, TNF-α and MDA in Groups B and C were lower than those of Groups D and E, respectively (P<0.01). Hydrogen-rich saline has anti-inflammatory and anti-oxidative effects in UHS. In conclusion, the results showed that itravenous injection of hydrogen-rich saline is more effective than intraperitonal injection.

Protective Effects of Hydrogen-Rich Saline Against Erectile Dysfunction in a Streptozotocin Induced Diabetic Rat Model

Protective Effects of Hydrogen-Rich Saline Against Erectile Dysfunction in a Streptozotocin Induced Diabetic Rat Model

Protective effects of hydrogen-rich saline against γ-ray irradiation-induced injury in kidney epithelial HK-2 cells

Protective effects of hydrogen-rich saline against γ-ray irradiation-induced injury in kidney epithelial HK-2 cells

Protective effects of hydrogen-rich saline on necrotizing enterocolitis in neonatal rats

PurposeThe aim of this study was to test the hypothesis that hydrogen-rich saline (HRS) might have protective effects on the development of necrotizing enterocolitis (NEC) in a neonatal rat model. MethodsNEC was induced in male newborn Sprague–Dawley rats by formula feeding, exposure to asphyxia and cold stress. Sixty-four rat pups were divided randomly into four groups: C+NS (n=11), C+H2 (n=11), NEC+NS (n=20), and NEC+H2 (n=22). Rats in the former two groups were mother-fed. Pups received intra-peritoneal injection of HRS (10ml/kg, 10min before asphyxia stress twice a day) or the same dose of normal saline. Rats were monitored until 96h after birth. Body weight, histological NEC score, survival time, malondialdehyde, antioxidant capacity, inflammatory mediators, and mucosal integrity were assessed. ResultsHRS treatment maintained the body weight, reduced the incidence of NEC from 85% (17/20) to 54.5% (12/22), increased the survival rate from 25% (5/20) to 68.2% (15/22), and attenuated the severity of NEC. In addition, HRS inhibited the mRNA expression of pro-inflammatory mediators (inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin-6), down-regulated lipid peroxidation, enhanced total antioxidant capacity, and prevented the increase of diamine oxidase in serum. However, no significant influence of HRS on the interleukin-10 mRNA expression was observed. ConclusionsHRS showed beneficial effects on neonatal rats with NEC via decreasing oxidative stress, increasing antioxidant capacity, suppressing inflammation, and preserving mucosal integrity.

Protective effects of hydrogen-rich saline on ulcerative colitis rat model

BackgroundUlcerative colitis (UC) is associated with enhanced production of reactive oxygen species and altered angiogenesis. Molecular hydrogen has been documented as a novel antioxidant to treat various reactive oxygen species-related diseases. The present study aimed to investigate the effects of hydrogen on UC using a rat model. Materials and methodsUC in rats was induced with intracolonically administrated acetic acid. Hydrogen was supplied through intraperitoneal injection of 10 or 20 mL/kg hydrogen-rich saline. The hydrogen treatment was performed once every 2 d and lasted 2 wk. The stool consistency and weight loss were used to evaluate UC development. Colonic mucosal damage at the end of the experiment was scored using the macroscopic and microscopic observations. Vascular endothelial growth factor expression in the colonic mucosa was determined using immunohistochemistry. ResultsThe administration of acetic acid induced acute rat UC, as indicated by diarrhea, weight loss, and colonic mucosal damage. Treatment with hydrogen-rich saline reduced the weight loss and diarrhea and alleviated the colonic mucosal damage in the UC rats. In addition, the expression of vascular endothelial growth factor in the UC rats increased and could be inhibited by hydrogen treatment. ConclusionsAntioxidative hydrogen-rich saline effectively protected the rats from UC, which might be, at least in part, because of inhibition of vascular endothelial growth factor.

Protective effects of hydrogen-rich saline on acute kidney injury in rats with sepsis

Objective To investigate the effects of hydrogen-rich saline (HRS) on acute kidney injury (AKI) in a rat model of sepsis.Methods Twenty-four male SD rats were randomly (random number) assigned to the sham operation group,the cecal ligation and puncture (CLP) group,and the CLP + HRS group (n =8).The rats in the sham operation group were treated with lapa(r ly) without CLP,while the rats in the CLP group and CLP + HRS group were made to be CLP-induced sepsis model.At 0,6 and 18 h after sham operation or CLP,rats in the CLP + HRS group received an intraperitoneal injection of HRS of 5 ml/kg,and 5 ml/kg of normal saline was given to the rats in the sham group and CLP group.Plasma levels of TNF-α,IL-6,IL-10,and HMGB1 were determined by enzyme linked immunosorbent assay (ELISA),plasma BUN and Cr were assayed by enzymatic assays,renal malondialdehyde (MDA) levels and superoxide dismutase (SOD) activities were determined by xanthine oxide method,renal tissue injury was dertermined by hematoxylin-eosin staining (liE),and renal cell apoptosis was assessed by terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) at 24 h after sham operation or CLP.Statistical analysis carried out by using one way analysis of variance followed by Student-Newman-Keuls (SNK) test.Results Compared with the sham group,rats in the CLP and CLP + HRS groups had increases in plasma levels of TNF-α,IL-6,IL-10,HMGB1,BUN,Cr,renal MDA,severe renal injury and apoptosis,and a decrease in renal SOD activities (P ＜ 0.05).Compared with the CLP group,the CLP + HRS group had decreases in plasma levels of HMGB1,BUN,renal MDA,mild renal injury and apoptosis,and an increase in renal SOD activities (P ＜ 0.05).Conclusions HRS reduces inflammatory reaction and oxidative stress,improving renal function during AKI in the rat model of sepsis. Key words: Hydrogen-rich saline ; Sepsis ; Inflammatory reaction ; Oxidative stress ; Acute kidney injury

Protective Effects of Hydrogen-Rich Saline Against Erectile Dysfunction in a Streptozotocin Induced Diabetic Rat Model

Hydrogen has antioxidative stress and anti-inflammatory effects. We investigated the effect of hydrogen on erectile dysfunction in streptozotocin induced diabetic rats. Diabetes was induced in Sprague-Dawley® rats by a single intravenous injection of streptozotocin. Diabetic rats were then randomized to a diabetes mellitus group and to a diabetic group that received hydrogen saline. The latter 8 rats were fed saturated hydrogen saline (5 ml/kg per day) by intragastric administration for 8 weeks. At the end of week 8 erectile function was assessed by measuring the increase in intracavernous pressure after cavernous nerve electrostimulation. We measured nitric oxide synthase activity, and malondialdehyde, 8-hydroxydeoxyguanosine, and nitrite and nitrate in the corpus cavernosum. eNOS protein immunolocalization in cavernous tissues was detected by immunohistochemistry. eNOS, Bcl-2 and Bax protein expression was determined by Western blot. We determined eNOS, Bcl-2 and Bax mRNA using real-time reverse transcriptase-polymerase chain reaction. Oxidative stress is involved in the pathophysiological mechanism of erectile dysfunction. Maximum intracavernous pressure in diabetic rats decreased significantly compared to controls and increased significantly compared to untreated diabetic rats after hydrogen-rich saline treatment. Decreased nitric oxide synthase activity, nitrite and nitrate, and eNOS expression as well as increased 8-hydroxydeoxyguanosine and malondialdehyde were found in the diabetic group compared to controls. Hydrogen-rich saline improved nitric oxide synthase activity, and malondialdehyde, nitrite and nitrate, and 8-hydroxydeoxyguanosine levels in the diabetic rat corpus cavernosum. Decreased eNOS in diabetic rats was ameliorated by hydrogen-rich saline. Also, apoptosis in the diabetic rat corpus cavernosum was significantly enhanced compared with controls. Hydrogen-rich saline therapy may decrease apoptosis in cavernous tissues and it ameliorated erectile dysfunction in diabetic rats by inhibiting oxidative stress and apoptosis. Hydrogen-rich saline effectively improved erectile function in a streptozotocin induced diabetic rat model of erectile dysfunction.

Protective effects of hydrogen-rich saline in a rat model of permanent focal cerebral ischemia via reducing oxidative stress and inflammatory cytokines

Hydrogen gas (H(2)) as a new medical gas exerts organ-protective effects through regulating oxidative stress, inflammation and apoptosis. In contrast to H(2), hydrogen-rich saline (HS) may be more suitable for clinical application. The present study was designed to investigate whether HS can offer a neuroprotective effect in a rat model of permanent focal cerebral ischemia and what mechanism(s) underlies the effect. Sprague-Dawley rats were subjected to permanent focal cerebral ischemia induced by permanent middle cerebral artery occlusion (pMCAO). Different doses of HS or normal saline were intraperitoneally administered at 5min after pMCAO or sham operation followed by injections at 6h, 12h and 24h. Here, we found that HS treatment significantly reduced infarct volume and improved neurobehavioral outcomes at 24h, 48h and 72h after pMCAO operation in a dose-dependent manner (P<0.05). Moreover, we found that HS treatment dose-dependently increased the activities of endogenous antioxidant enzymes (SOD and CAT) as well as decreased the levels of oxidative products (8-iso-PGF2α and MDA) and inflammatory cytokines (TNF-α and HMGB1) in injured ipsilateral brain tissues at 6h, 12h and 24h after pMCAO operation (P<0.05). Thus, hydrogen-rich saline dose-dependently exerts a neuroprotective effect against permanent focal cerebral ischemia, and its beneficial effect is at least partially mediated by reducing oxidative stress and inflammation. Molecular hydrogen may be an effective therapeutic strategy for stroke patients.

Hydrogen-rich saline protects against oxidative damage and cognitive deficits after mild traumatic brain injury

Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates events that result in protracted neuronal dysfunction and remodeling. Importantly, antioxidants can protect the brain against oxidative damage and modulate the capacity of the brain to cope with synaptic dysfunction and cognitive impairment. However, no studies have investigated the effects of hydrogen-rich saline on cognitive deficits after TBI. In the present study, rats with fluid percussion injury (FPI) were used to investigate the protective effects of hydrogen-rich saline. The results showed that hydrogen-rich saline reduced the level of malondialdehyde (MDA) and elevated the level of silent information regulator 2 (Sir2). In addition, treatment with hydrogen-rich saline, which elevated the levels of molecules associated with brain-derived neurotropic factor (BDNF)-mediated synaptic plasticity, improved cognitive performance in the Morris water maze after mild TBI. These results suggest that hydrogen-rich saline can protect the brain against the deleterious effects of mild TBI on synaptic plasticity and cognition and that hydrogen-rich saline could be an effective therapeutic strategy for patients with cognitive deficits after TBI.

Protective effects of hydrogen-rich saline in a rat model of traumatic brain injury via reducing oxidative stress

BackgroundHydrogen gas (H2) has been considered as a novel antioxidant to selectively reduce the toxic reactive oxygen species (ROS) such as hydroxyl radical (•OH) without affecting the other signal ROS. Our recent study shows that H2 inhalation is beneficial to traumatic brain injury (TBI) via reducing oxidative stress. In contrast to H2, hydrogen-rich saline (HS) may be more suitable for clinical application. The present study was designed to investigate whether HS has a protective effect against TBI via reducing oxidative stress in rats. MethodsTBI model was induced by controlled cortical impact injury. Different dosages of HS were intraperitoneally administered at 5 min after TBI operation. We then measured the brain edema, blood-brain barrier (BBB) breakdown, neurological dysfunction and injury volume in all animals. In addition, the oxidative products and antioxidant enzymes in brain tissues were detected. ResultsTBI-challenged rats exhibited significant brain injuries characterized by the increase of BBB permeability, brain edema, and lesion volume as well as neurological dysfunction, which were dose-dependently ameliorated by HS treatment. Moreover, we found that HS treatment increased the endogenous antioxidant enzymatic activities and decreased the oxidative product levels in brain tissues of TBI-challenged rats. ConclusionHydrogen-rich saline can exert a protective effect against TBI via reducing oxidative stress. Molecular hydrogen may be a more effective therapeutic strategy for TBI patients.

Protective effects of hydrogen-rich saline on monocrotaline-induced pulmonary hypertension in a rat model

BackgroundHydrogen-rich saline has been reported to have antioxidant and anti-inflammatory effects and effectively protect against organ damage. Oxidative stress and inflammation contribute to the pathogenesis and/or development of pulmonary hypertension. In this study, we investigated the effects of hydrogen-rich saline on the prevention of pulmonary hypertension induced by monocrotaline in a rat model.MethodsIn male Sprague-Dawley rats, pulmonary hypertension was induced by subcutaneous administration of monocrotaline at a concentration of 6 mg/100 g body weight. Hydrogen-rich saline (5 ml/kg) or saline was administred intraperitoneally once daily for 2 or 3 weeks. Severity of pulmonary hypertension was assessed by hemodynamic index and histologic analysis. Malondialdehyde and 8-hydroxy-desoxyguanosine level, and superoxide dismutase activity were measured in the lung tissue and serum. Levels of pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6) in serum were determined with enzyme-linked immunosorbent assay.ResultsHydrogen-rich saline treatment improved hemodynamics and reversed right ventricular hypertrophy. It also decreased malondialdehyde and 8-hydroxy-desoxyguanosine levels, and increased superoxide dismutase activity in the lung tissue and serum, accompanied by a decrease in pro-inflammatory cytokines.ConclusionsThese results suggest that hydrogen-rich saline ameliorates the progression of pulmonary hypertension induced by monocrotaline in rats, which may be associated with its antioxidant and anti-inflammatory effects.

Protective effects of hydrogen-rich saline in preeclampsia rat model

Hydrogen has been reported as a novel antioxidant to selectively reduce levels of toxic reactive-oxygen species (ROS). We investigated the effects of hydrogen-rich saline on the prevention of oxidative injuries in N(omega)-nitro-l-arginine methyl ester (l-NAME) induced rat model of preeclampsia (PE). Sprague–Dawley rats (n = 50) were randomized into five groups: non-pregnant; normal pregnancy; pregnancy + hydrogen saline, 5 ml/kg, intraperitoneal (i.p.); pregnancy + l-NAME, 60 mg/kg (i.p.); pregnancy + l-NAME + hydrogen saline rats. Terminations of pregnancy were performed on day 22 of gestation, when the placentas and kidneys were microscopically inspected; tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and malonyldialdehyde (MDA) were assessed; and the mean systolic BP, level of proteinuria, resorptions, and pups birth weights were recorded. It was found that the pups of hypertensive gravid rats treated with hydrogen-rich saline presented fewer number of resorptions than those of the group of pregnancy + l-NAME, 60 mg/kg i.p. (P < 0.05). Additionally, hydrogen-rich saline treatment decreased the blood and placental MDA, proteinuria and the pro-inflammatory cytokine TNF-α, IL-1β in the placental tissues compared with those in L-NAME-treated rats (all P < 0.05). The mean systolic BP showed no significant difference except on day 22 of gestation (P < 0.05). The preventive administration of hydrogen significantly attenuated the severity of PE, which might be ascribed to a reduction in inflammation response and oxidative stress. It could be concluded that hydrogen can be an effective antioxidant in the management of PE.

Protective effects of hydrogen-rich saline against hind limb ischemia reperfusion injury and associated remote lung injury

Objective To explore the protective effects of hydrogen-rich saline against hind limb ischemia reperfusion injury and associated remote lung injury in rats. Methods Thirty Sprague-Dawley rats were randomly divided into three groups: sham group ( group S) ; saline control group (group C) , undergoing intravenous infusion of saline (1 ml/100 g) at 10 min before reperfusion; hydrogen-treated group ( group H) , undergoing intravenous infusion of hydrogen-rich saline (1 ml/100 g) at 10 min before reperfusion. Hind limb ischemia reperfusion model was established by 4 h of the abdominal aorta ligation followed by a 4 h of reperfusion. Rats were killed at the end of reperfusion, and blood samples were collected for determination of serum levels of tumor necrosis factor-α ( TNF-α) , interleukin-6 (IL-6) and malonyldialdehyde ( MDA). Specimens of lung and gastrocnemius muscle were collected for measurement of wet-todry weight (W/D) ratio, light microscopic examination and detection of plasma TNF-α, IL-6 and MDA.Results The pathological changes were milder in group H than in group C. The lung (4. 47 ±0. 23) and gastrocnemius muscle (4. 04 ±0. 22) W/D ratio in group H was significantly lower than in group C (4. 67 ±0.27 vs4. 67 ±0.27, P＜0.05). The serum [(2.08 ± 1. 27) μmol/L, (528. 22 ±221. 17) , (41.14± 13. 01) ng/L, respectively] and homogenate levels [(3. 58 ± 1. 62) μmol/L, ( 1. 17 ±0. 15) , (0. 79±0.29) ng/L in the lung; (8.91 ±3. 13) μmol/L, (3. 13 ±0. 41) ,(3. 07 ± 1. 69) ng/L in the gastrocnemius muscle, respectively] of MDA, IL-6 and TNF-a were also significantly lower in group H than in group C (P ＜0. 05) , but there was no significant difference from group S. Conclusion Infusion of hydrogen-rich saline before reperfsion significantly alleviates the hind limb ischemia reperfusion injury and associated remote lung injury. Key words: Hydrogen-rich saline; Lung; Skeletal muscle; Reperfusion injury; Free radicals