Publications (20)39.27 Total impact
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Article: Xenon preconditioning: molecular mechanisms and biological effects.
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ABSTRACT: Xenon is one of noble gases and has been recognized as an anesthetic for more than 50 years. Xenon possesses many of the characteristics of an ideal anesthetic, but it is not widely applied in clinical practice mainly because of its high cost. In recent years, numerous studies have demonstrated that xenon as an anesthetic can exert neuroprotective and cardioprotective effects in different models. Moreover, xenon has been applied in the preconditioning, and the neuroprotective and cardioprotective effect of xenon preconditioning have been investigated in a lot of studies in which some mechanisms related to these protections are proposed. In this review, we summarized these mechanisms and the biological effects of xenon preconditioning.Medical gas research. 01/2013; 3(1):3. -
Article: Is methane a new therapeutic gas?
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ABSTRACT: BACKGROUND: Methane is an attractive fuel. Biologically, methanogens in the colon can use carbon dioxide and hydrogen to produce methane as a by-product. It was previously considered that methane is not utilized by humans. However, in a recent study, results demonstrated that methane could exert anti-inflammatory effects in a dog small intestinal ischemia-reperfusion model. POINT OF VIEW: Actually, the bioactivity of methane has been investigated in gastrointestinal diseases, but the exact mechanism underlying the anti-inflammatory effects is required to be further elucidated. Methane can cross the membrane and is easy to collect due to its abundance in natural gas. Although methane is flammable, saline rich in methane can be prepared for clinical use. These seem to be good news in application of methane as a therapeutic gas. CONCLUSION: Several problems should be resolved before its wide application in clinical practice.Medical gas research. 09/2012; 2(1):25. -
Article: Nrf2 as a converging node for cellular signaling pathways of gasotransmitters.
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ABSTRACT: Gasotransmitters is a family of endogenous molecules of gases or gaseous signaling molecules. To date, nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) have been found to be important gasotransmitters in humans. Three gasotransmitters at high concentrations have been confirmed to be detrimental to human health, while evidence shows they at low concentrations may confer protective effects. There are important interactions among three gasotransmitters. Recent evidence reveals that these gasotransmitters may converge at Nrf2, an important transcription factor able to induce the expressions of some critical antioxidant enzymes, which may attribute to the protective effects of these gasotransmitters. Thus, we hypothesize that Nrf2 serves as a converging node for cellular signaling pathways of gasotransmitters, which adds evidence on the interactions among them.Medical Hypotheses 06/2012; 79(3):308-10. · 1.39 Impact Factor -
Article: Hyperoxia preconditioning: the next frontier in neurology?
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ABSTRACT: Oxygen is indispensable for all aerobic organisms and has become one of the most widely used therapeutic agents. Currently, oxygen not only is applied in the treatment of diseases, but becomes a modality for the prevention of some diseases. Hyperoxia preconditioning with normobaric or hyperbaric oxygen has been found to be protective in some diseases in several animal models and clinical trials. Currently, investigators pay increasing attention to the application of hyperoxia preconditioning in the prevention of common neurological diseases, and encouraging effectiveness has been achieved. In the present short review, we briefly described the development, application and mechanisms of hyperoxia preconditioning in the neurology, and the issues in future application of hyperoxia preconditioning were also proposed.Neurological Research 05/2012; 34(5):415-21. · 1.52 Impact Factor -
Article: Effects of hyperbaric oxygen on uric acid and arachidonic acid: a metabolomic study in rats and humans
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ABSTRACT: Hyperoxia is routinely used to prevent or treat hypoxemia and acute respiratory failure, and sustain aerobic life in military and commercial operations. However, breathing oxygen acutely at high pressures and for long durations is toxic. The present study aimed to investigate effects of hyperbaric oxygen (HBO) exposure on plasma metabolite profiles. We applied a liquid chromatography-mass spectrometry based metabolomic approach to analyze metabolites from plasma of both rats and humans under HBO conditions to explore the possible effects of HBO on the body. Uric acid (UA) and arachidonic acid concentrations were changed significantly in both rat and human plasma, and some precursor metabolites of UA in the UA pathway were also changed. For acute and chronic HBO exposures on plasma UA after exogenous UA injection, the results indicated exogenous administration of UA significantly increased plasma UA and ascorbic acid levels. However, these returned to normal levels 48h after HBO exposure. These findings suggest HBO exposure can combat the harmful effects of increased UA from exposure to elevated partial pressure of oxygen. Furthermore, exogenous administration of UA not only does not disturb its metabolism, but also increases its anti-oxidative capacity (increase ascorbic acid). These findings suggest that the use of antioxidants might be necessary under HBO exposure, especially under extreme HBO exposure. KeywordsHyperbaric oxygen-Metabolomics-Uric acid-Arachidonic acid-Oxygen toxicityMetabolomics 04/2012; 6(3):375-385. · 4.51 Impact Factor -
Article: Cyclooxygenase-2 mediates hyperbaric oxygen preconditioning in the rat model of transient global cerebral ischemia.
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ABSTRACT: Hyperbaric oxygen (HBO) preconditioning (PC) allows brain protection against transient global ischemia. In the present study, we hypothesize that the mechanism of HBO-PC involves the induction of cyclooxygenase-2 (COX-2) in cerebral tissues before ischemia, which leads to a suppression of COX-2 and its downstream targets after global ischemic insult. One hundred twenty-nine male Sprague Dawley rats (body weight 280-300 grams) were allocated to the naive control group and the sham operation group, and 3 groups of animals were subjected to 15-minute 4-vessel occlusion: untreated, preconditioned with HBO 2.5 atmospheres absolutes for 1 hour daily for 5 days, preconditioned as mentioned and administered with COX-2 inhibitor NS-398 (1 mg/kg body weight intraperitoneal) before each preconditioning session, and normal rats preconditioned with HBO without ischemia. The mortality, the incidence of seizures, and T-maze scores were recorded. The quantitative cell count in Nissl stain and TUNEL was conducted on day 7 after ischemia. The brain expression of COX-2 was analyzed with Western blotting and immunofluorescence staining. HBO-PC increased the number of surviving neurons in the Cornu Ammonis area 1, which was associated with the reduced COX-2 expression in the hippocampus and in the cerebral cortex at 1 and 3 days after ischemia. HBO-PC improved functional performance and tended to decrease mortality and the frequency of seizures. These beneficial effects of HBO-PC were abolished by the COX-2 selective inhibitor NS-398. HBO-PC reduced COX-2 expression and provided brain protection after global ischemia. Administration of COX-2 inhibitor with HBO before ischemia abolished preconditioning effect, thereby implicating COX-2 as a mediator of HBO-PC in the ischemic brain.Stroke 02/2011; 42(2):484-90. · 5.73 Impact Factor -
Article: Helium preconditioning attenuates hypoxia/ischemia-induced injury in the developing brain.
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ABSTRACT: Recent studies show helium may be one kind of neuroprotective gas. This study aimed to examine the short and long-term neuroprotective effects of helium preconditioning in an established neonatal cerebral hypoxia-ischemia (HI) model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min of hypoxia (8% oxygen at 37°C). The preconditioning group inhaled 70% helium-30% oxygen for 5 min three times with an interval of 5 min 24h before HI insult. Pups were decapitated 24h after HI and brain morphological injury was assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining, Nissl and TUNEL staining. Caspase-3 activity in the brain was measured. Five weeks after HI, postural reflex testing and Morris water maze testing were conducted. Our results showed that helium preconditioning reduced the infarct ratio, increased the number of survival neurons, and inhibited apoptosis at the early stage of HI insult. Furthermore, the sensorimotor function and the cognitive function were improved significantly in rats with helium preconditioning. The results indicate that helium preconditioning attenuates HI induced brain injury.Brain research 02/2011; 1376:122-9. · 2.46 Impact Factor -
Article: Protective effects of hydrogen on fetal brain injury during maternal hypoxia.
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ABSTRACT: This study aimed to investigate the effects of hydrogen on fetal brain injury during maternal hypoxia. Pregnant rats (n=12, at gestational day 17) were randomly assigned into three groups; air, hypoxia, and hypoxia plus hydrogen groups were put into a chamber and flushed with room air (21% O2 and 79% N2), hypoxia (8% O2 and 92% N2), and hypoxia with hydrogen mixture (2% H2, 8% O2 and 90% N2), respectively, for 4 consecutive hours. After birth, body and brain weights, body-righting reflex, and negative geotropism of neonates were measured, and then pups were killed at days 1 and 7. Oligodendrocytes were studied at post-natal day 1 by immunohistochemistry. We found significant decreases in body weight in the hypoxia group (P<0.05 vs. room air group), but not in the hypoxia plus hydrogen group (P>0.05 vs. room air group). Even though brain weight was not different among groups, the brain weight to body weight ratio in the room air group was significantly (P<0.05) lower than that in the hypoxia alone or hypoxia plus hydrogen groups. Body-righting reflex at day 1 and negative geotropism at days 3-4 showed deficiency in hypoxia animals when compared with the room air group (P<0.05). Hydrogen treatment improved the body-righting reflex and negative geotropism (P<0.05 vs. room air group). The above-mentioned functional changes caused by hypoxia were not associated with morphology and cell death of oligodendrocytes. Therefore, the maternal hypoxia-induced body weight loss, and functional abnormalities and hydrogen treatment during hypoxia offered a protective effect and improved functions in neonates.Acta neurochirurgica. Supplement 01/2011; 111:307-11. -
Article: Application of medical gases in the field of neurobiology.
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ABSTRACT: Medical gases are pharmaceutical molecules which offer solutions to a wide array of medical needs. This can range from use in burn and stroke victims to hypoxia therapy in children. More specifically however, gases such as oxygen, helium, xenon, and hydrogen have recently come under increased exploration for their potential theraputic use with various brain disease states including hypoxia-ischemia, cerebral hemorrhages, and traumatic brain injuries. As a result, this article will review the various advances in medical gas research and discuss the potential therapeutic applications and mechanisms with regards to the field of neurobiology.Medical gas research. 01/2011; 1(1):13. -
Article: Hydrogen saline offers neuroprotection by reducing oxidative stress in a focal cerebral ischemia-reperfusion rat model.
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ABSTRACT: Hydrogen gas is neuroprotective in cerebral ischemia animal models. In this study, we tested the neuroprotective effects of hydrogen saline, which is safe and easy to use clinically, in a rat model of middle cerebral artery occlusion (MCAO). Sprague-Dawley male rats weighting 250-280 g were divided into sham, MCAO plus hydrogen saline and MCAO groups, and subjected to 90-min ischemia followed by 24 h of reperfusion. Hydrogen saline was injected intraperitoneally at 1 ml/100 g body weight. Infarct volume and brain water content were evaluated at different time points after reperfusion. Oxidative stress, inflammation, and apoptotic cell death markers were measured. Hydrogen saline significantly reduced the infarct volume and edema and improved the neurological function, when it was administered at 0, 3 and 6 h after reperfusion. Hydrogen saline decreased 8-hydroxyl-2'-deoxyguanosine (8-OHdG), reduced malondidehyde, interleukin-1β, tumor necrosis factor-α, and suppressed caspase 3 activity in the ischemic brain. These findings demonstrated hydrogen saline is neuroprotective when administered within 6 h after ischemia. Because hydrogen saline is safe and easy to use, it has clinical potentials to reduce neurological injuries.Medical gas research. 01/2011; 1(1):15. -
Article: Consumption of hydrogen water reduces paraquat-induced acute lung injury in rats.
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ABSTRACT: Exposure to paraquat leads to acute lung injury and oxidative stress is widely accepted as a contributor to paraquat-induced acute lung injury. Recent studies have reported that consumption of water with dissolved molecular hydrogen to a saturated level (hydrogen water) prevents oxidative stress-induced diseases. Here, we investigated whether consumption of saturated hydrogen saline protects rats against paraquat-induced acute lung injury. Adult male Sprague-Dawley (SD) rats were randomly divided into four groups: Control group; hydrogen water-only group (HW group); paraquat-only group (PQ group); paraquat and hydrogen water group (PQ + HW group). The rats in control group and HW group drank pure water or hydrogen water; the rats in PQ group and PQ + HW group were intraperitonealy injected with paraquat (35 mg/kg) and then provided pure water or hydrogen water. Both biochemical and histological lung alterations were measured. The results showed that hydrogen water ameliorated these alterations, demonstrating that hydrogen water alleviated paraquat-induced acute lung injury possibly by inhibition of oxidative damage.Journal of Biomedicine and Biotechnology 01/2011; 2011:305086. · 2.44 Impact Factor -
Article: Sulforaphane protects brains against hypoxic-ischemic injury through induction of Nrf2-dependent phase 2 enzyme.
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ABSTRACT: Neonatal hypoxia-ischemia (HI) brain injury involves reactive oxygen species (ROS) and inflammatory responses. Sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, has cytoprotective effects against oxidative stress and its effect was mediated by NF-E2-related factor-2 (Nrf2), a transcription factor, and heme oxygenase 1 (HO-1) which is one of Nrf2 downstream target genes. This study was undertaken to investigate the neuroprotective mechanisms of SFN in a neonatal HI rat model. Seven-day-old rat pups were subjected to left common carotid artery ligation and hypoxia (8% oxygen at 37 degrees C) for 90 min. SFN (5mg/kg) was systemically administered 30 min before HI insult. Brain injury was assessed by 2,3,5-triphenyltetrazoliumchloride (TTC), Nissl, TUNEL staining, malondialdehyde (MDA), 8OH-dG level, and caspase-3 activity in the cortex and hippocampus. SFN pretreatment increased the expression of Nrf2 and HO-1 in the brain and reduced infarct ratio at 24h after HI. The number of TUNEL-positive neurons as well as activated macroglia and the amount of 8OH-dG, were markedly reduced after SFN treatment, accompanied by suppressed caspase-3 activity and reduced lipid peroxidation (MDA) level. These results demonstrated that SFN could exert neuroprotective effects through increasing Nrf2 and HO-1 expression.Brain research 07/2010; 1343:178-85. · 2.46 Impact Factor -
Article: Recombinant osteopontin attenuates brain injury after intracerebral hemorrhage in mice.
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ABSTRACT: Osteopontin (OPN), an extracellular matrix glycoprotein, has been reported to inhibit inducible nitric oxide synthase (iNOS). We examined if recombinant OPN (r-OPN) inhibits iNOS and prevents brain injury in a mouse collagenase-induced intracerebral hemorrhage (ICH) model. One hundred one mice were randomly assigned to five groups: sham, ICH + vehicle, ICH + r-OPN (10, 50, or 100 ng per mouse) groups. Vehicle or r-OPN was administered via an intracerebroventricular infusion 20 min pre-ICH. Neurological scores and brain water content were evaluated at 24 and 72 h, and hemoglobin assay, Nissl staining and Western blot for iNOS, Stat1, matrix metalloproteinase (MMP)-9 and zonula occludens (ZO)-1 were performed at 24 h post-ICH. r-OPN did not affect hematoma formation. Middle (50 ng)- and high (100 ng)-dose, but not low (10 ng)-dose of r-OPN treatment significantly improved neurological scores and brain water content compared with the vehicle group. The protective effect of r-OPN was associated with significantly rescued neuronal cells in the peri-hematoma region as well as a decrease in the Stat1 phosphorylation, iNOS induction, MMP-9 activation, and ZO-1 degradation. This study suggests that r-OPN may down-regulate iNOS expression by the inhibition of Stat1 phosphorylation, and therefore suppressing the MMP-9 activation, preventing ICH-induced brain injury in mice.Neurocritical Care 05/2010; 14(1):109-17. · 2.47 Impact Factor -
Article: Hydrogen-rich saline protects myocardium against ischemia/reperfusion injury in rats.
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ABSTRACT: Protective effect of hydrogen (H(2)) gas on cardiac ischemia-reperfusion (I/R) injury has been demonstrated previously. This study was designed to test the hypothesis that hydrogen-rich saline (saline saturated with molecular hydrogen), which is easy to use, induces cardioprotection against ischemia (30 min) and reperfusion (24 h) injury in rats. Adult male Sprague-Dawley rats underwent 30-min occlusion of the left anterior descending (LAD) coronary artery and 24-h reperfusion. Intraperitoneal injection of hydrogen-rich saline before reperfusion significantly decreased plasma and myocardium malondialdehyde (MDA) concentration, decreased cardiac cell apoptosis, and myocardial 8-hydroxydeoxyguanosine (8-OHdG) in area at risk zones (AAR), suppressed the activity of caspase-3, and reduced infarct size. The heart function parameters including left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVDP), +(dP/dt)(max) and -(dP/dt)(max) were also significantly improved 24 h after reperfusion. It is concluded that hydrogen-rich saline is a novel, simple, safe, and effective method to attenuate myocardial I/R injury.Experimental Biology and Medicine 08/2009; 234(10):1212-9. · 2.64 Impact Factor -
Article: Hydrogen-rich saline protects against intestinal ischemia/reperfusion injury in rats.
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ABSTRACT: Hydrogen gas was reported to reduce reactive oxygen species and alleviate cerebral, myocardial and hepatic ischemia/reperfusion (I/R) injuries. This paper studied the effect of hydrogen-rich saline, which was easier for clinical application, on the intestinal I/R injury. Model of intestinal I/R injury was induced in male Sprague-Dawley rats. Physiological saline, hydrogen-rich saline or nitrogen-rich saline (5 ml/kg) was administered via intravenous infusion at 10 min before reperfusion, respectively. The intestine damage was detected microscopically and was assessed by Chiu score system after I/R injury. In addition, serum DAO activity, TNF-alpha, IL-1beta and IL-6 levels, tissue MDA, protein carbonyl and MPO activity were all increased significantly by I/R injury. Hydrogen-rich saline reduced these markers and relieved morphological intestinal injury, while no significant reduction was observed in the nitrogen-rich saline-treated animals. In conclusion, hydrogen-rich saline protected the small intestine against I/R injury, possibly by reduction of inflammation and oxidative stress.Free radical research 05/2009; 43(5):478-84. · 2.22 Impact Factor -
Article: Neuroprotective effects of hydrogen saline in neonatal hypoxia-ischemia rat model.
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ABSTRACT: Cerebral hypoxia-ischemia (HI) represents a major cause of brain damage in the term newborn. This study aimed to examine the short and long-term neuroprotective effect of hydrogen saline (H(2) saline) using an established neonatal HI rat pup model. Seven-day-old rat pups were subjected to left common carotid artery ligation and then 90 min hypoxia (8% oxygen at 37 degrees C). H(2) saturated saline was administered by peritoneal injection (5 ml/kg) immediately and again at 8 h after HI insult. At 24 h after HI, the pups were decapitated and brain morphological injury was assessed by 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, and TUNEL staining. Acute cell death, inflammation and oxidative stress were evaluated at 24 h by studying caspase-3 activity, MDA measurement as well as Iba-1 immunochemistry in the brain. At 5 weeks after HI, spontaneous activity test and Morris water maze test were conducted. We observed that H(2) saline treatment reduced the caspase activity, MDA, Iba-1 levels, the infarct ratio, and improved the long-term neurological and neurobehavioral functions. H(2) saline has potentials in the clinical treatment of HI and other ischemia-related cerebral diseases.Brain research 12/2008; 1256:129-37. · 2.46 Impact Factor -
Article: Hyperbaric oxygen preconditioning induces tolerance against brain ischemia-reperfusion injury by upregulation of antioxidant enzymes in rats.
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ABSTRACT: The present study examined the hypothesis that cerebral ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is associated with an increase of antioxidant enzyme activity. Male Sprague-Dawley rats (250-280 g, n=74) were divided into sham, middle cerebral artery occlusion (MCAO) for 90 min, and MCAO plus HBO-PC groups. HBO-PC was conducted four times by given 100% oxygen at 2.5 atmosphere absolute (ATA), for 1 h at every 12 h interval for 2 days. At 24 h after the last HBO-PC, MCAO was performed and at 24 h after MCAO, neurological function and Nissl Staining were performed to evaluate the effect of HBO-PC. Malondialdehyde (MDA) content, activity of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) sampled from the hippocampus, ischemic penumbra or core of cortex were measured. HBO-PC decreased mortality rate, improved neurological recovery, lessened neuronal injury, reduced the level of MDA and increased the antioxidant activity of CAT and SOD. These observations demonstrated that an upregulation of the antioxidant enzyme activity by HBO preconditioning plays an important role in the generation of tolerance against brain ischemia-reperfusion injury.Brain Research 06/2008; 1210:223-9. · 2.73 Impact Factor -
Article: Repetitive hyperbaric oxygen exposures enhance sensitivity to convulsion by upregulation of eNOS and nNOS.
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ABSTRACT: Repetitive hyperbaric oxygen (HBO) exposures as preconditioning methods produce ischemic tolerance, but may increase the risk of convulsions in patients. The purpose of this study was to investigate the mechanisms in increased sensitivity to convulsions and the role of nitric oxide (NO) and its synthases after repetitive HBO exposures. Mice were randomly assigned into three groups: HBO group, hyperbaric air (HBA) group and normobaric air (NBA) group. Mice in HBO or HBA group were exposed to hyperbaric oxygen or hyperbaric air respectively for 60 min twice daily for 3 consecutive days (2.5 atmosphere absolute [ATA]). 24 h after the last exposure, mice were exposed to HBO (100% O2, 6 ATA). The latency of convulsions was recorded. In addition, the levels of NO, NADPH-diaphorase, mRNA and protein expressions of NOS isoforms in hypothalamus and hippocampus were determined. Latency to seizures was significantly shortened in mice after six HBO pre-exposures. The level of NO in hypothalamus in HBO group was increased. The number of NADPH-d positive cells and the levels of protein and mRNA of eNOS and nNOS in hypothalamus and hippocampus were increased. After repeated HBO exposures, elevated NO may enhance the sensitivity to convulsions and this may lead to seizures during the subsequent oxygen exposures. Prevention of seizures is needed when HBO is used as preconditioning method.Brain Research 04/2008; 1201:128-34. · 2.73 Impact Factor -
Article: Mechanism of hyperbaric oxygen preconditioning in neonatal hypoxia-ischemia rat model.
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ABSTRACT: Hypoxic ischemic (HI) injury in neonates damages brain tissues. We examined the mechanism of hyperbaric oxygen preconditioning (HBO-PC) in neonatal HI rat model. Seven-day-old rat pups were subjected to left common carotid artery ligation and hypoxia (8% oxygen at 37 degrees C) for 90 min. HBO (100% O(2), 2.5 atmospheres absolute for 2.5 h) were administered by placing pups in a chamber 24 h before HI insult. Brain injury was assessed by the survival rate, 2,3,5-triphenyltetrazolium chloride (TTC), Nissl, TUNEL straining and caspase-3,caspase-9 activities after HI. In HBO preconditioned animals, survival rate was increased, infarct ratio was decreased, and the positive stained TUNEL cells were reduced, accompanied by the suppression of caspase-3 and -9 activities. These results indicate that a single HBO-PC appears to provide brain protection against HI insult via inhibition of neuronal apoptosis pathways.Brain Research 03/2008; 1196:151-6. · 2.73 Impact Factor -
Article: Saturated hydrogen saline protects the lung against oxygen toxicity.
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ABSTRACT: Exposure to high oxygen concentrations leads to acute lung injury, including lung tissue and alveolar edema formation, congestion, intra-alveolar hemorrhage, as well as endothelial and epithelial cell apoptosis or necrosis. Several studies have reported that molecular hydrogen is an efficient antioxidant by gaseous rapid diffusion into tissues and cells. Moreover, consumption of water with dissolved molecular hydrogen to a saturated level (hydrogen water) prevents stress-induced cognitive decline in mice and superoxide formation in mice. The purpose of the present study was to investigate the effect of saturated hydrogen saline on pulmonary injury-induced exposure to >98% oxygen at 2.5 ATA for five hours. Adult male Sprague-Dawley (SD) rats were randomly divided into three groups: control group, saline group and saturated hydrogen saline group. Hematoxylin and eosin (H&E) staining were used to examine histological changes. The lung wet to dry (W/D) weight ratio was calculated. The concentration of protein and total cell counts in bronchoalveolar lavage fluid (BALF) were measured. Lactate dehydrogenase (LDH) in serum and BALF were measured by spectrophotometer. The light microscope findings showed that saturated hydrogen saline reduced the impairment when compared with the saline group: Saturated hydrogen saline decreased lung edema, reduced LDH activity in BALF and serum, and decreased total cells and protein concentration in BALF. These results demonstrated that saturated hydrogen saline alleviated hyperoxia-induced pulmonary injury, which was partly responsible for the inhibition of oxidative damage.Undersea & hyperbaric medicine: journal of the Undersea and Hyperbaric Medical Society, Inc 37(3):185-92. · 0.80 Impact Factor
Top co-authors
Top Journals
Institutions
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2008–2012
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Second Military Medical University, Shanghai
- Faculty of Naval Medicine
Shanghai, Shanghai Shi, China -
Changhai Hospital, Shanghai
Shanghai, Shanghai Shi, China -
The Second Military Medical University
Shanghai, Shanghai Shi, China
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2009–2011
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Loma Linda University
- Division of Pharmacology
Loma Linda, CA, USA
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