Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 25
Filtrar
1.
Protoplasma ; 259(5): 1271-1282, 2022 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-35039948

RESUMEN

Oryza sativa PHOSPHATE RESPONSE2 (OsPHR2) can promote the uptake and use of phosphorus (P) in rice. We introduced OsPHR2 into the winter wheat (Triticum aestivum L.) variety "Zhengmai0856." OsPHR2 was integrated into the wheat genome with two copy numbers and could be correctly transcribed and expressed. OsPHR2 was mainly expressed in the leaves at the seedling stage. From the jointing to filling stage, OsPHR2 was mainly expressed in the roots, followed by the leaves, with a low expression level in detected the tassels and stems. The transgenic lines exhibited higher P accumulation at each growth stage and increased P uptake intensity in comparison to the wild type under low P and high P conditions. Analysis of the root characteristics showed that the transgenic expression of OsPHR2 increased the maximum root length, total root length, root-to-shoot ratio, and root volume under the conditions of P deficiency or low P. A field experiment showed that the transgenic lines had a higher grain yield than the wild type under low P and high P conditions. The yield of the transgenic lines increased by 6.29% and 3.73% on average compared with the wild type under low P and high P conditions, respectively. Thus, the transgenic expression of OsPHR2 could increase P uptake and yield in wheat, but the effect was more prominent under low P conditions.


Asunto(s)
Oryza , Transporte Biológico , Oryza/genética , Oryza/metabolismo , Fosfatos/metabolismo , Fósforo/metabolismo , Triticum/metabolismo
2.
Diving Hyperb Med ; 50(4): 343-349, 2020 Dec 20.
Artículo en Inglés | MEDLINE | ID: mdl-33325014

RESUMEN

INTRODUCTION: The lung is among the primary organs involved in decompression sickness (DCS). Xuebijing (XBJ), a traditional Chinese medicine, has been widely used in the treatment of various acute lung diseases. This study aimed to explore potential benefit of XBJ on lung injuries induced by DCS in a rabbit model. METHODS: Twenty-four male New Zealand white rabbits underwent a simulated air dive to 50 meters' sea water for 60 min with 2.5 min decompression, and received an intravenous injection of XBJ (5 ml·kg-1) or an equal volume of saline immediately following decompression. DCS signs were monitored for 24 h, and blood was sampled before simulated diving and at 6 h and 12 h following decompression for determination of inflammatory indices. Lung tissues were sampled after euthanasia for histology analysis and lung water content, as well as tumour necrosis factor-α level. Another six rabbits were used as control. RESULTS: XBJ significantly ameliorated lung injuries (lung wet/dry ratio and total protein content in bronchoalveolar lavage fluid), and notably inhibited systemic (serum level of interleukin-1ß) and local (tumour necrosis factor-α in bronchoalveolar lavage fluid) inflammation responses. CONCLUSIONS: The results strongly suggest the benefits of XBJ on ameliorating DCS lung injuries, which is possibly via inhibiting systemic and local inflammation. XBJ may be a potential candidate for the treatment of decompression-induced lung injuries.


Asunto(s)
Enfermedad de Descompresión , Medicamentos Herbarios Chinos , Lesión Pulmonar , Animales , Descompresión , Enfermedad de Descompresión/tratamiento farmacológico , Medicamentos Herbarios Chinos/farmacología , Pulmón , Lesión Pulmonar/prevención & control , Masculino , Conejos
3.
Diving Hyperb Med ; 48(4): 235-240, 2018 Dec 24.
Artículo en Inglés | MEDLINE | ID: mdl-30517956

RESUMEN

BACKGROUND: Recent studies indicated that ketone ester R,S-1,3-butanediol acetoacetate diester (BD-AcAc2) may be effective in preventing central nervous system oxygen toxicity (CNS-OT) and concomitant acute lung injury, a serious medical problem to be faced when breathing hyperbaric oxygen (HBO). This study aimed to further investigate the protective effects of BD-AcAc2 against CNS-OT and concomitant acute lung injury (ALI) in mice. METHODS: Mice were treated with BD-AcAc2 in peanut oil vehicle (2.5, 5.0 or 10.0 g·kg⁻² body weight) by gavage 20 minutes before 600 kPa HBO exposure. Control mice received the vehicle only. Seizure latency was recorded. Malondialdehyde content in brain and lung tissues, total protein level in bronchoalveolar lavage fluid (BLF) and lung water content were measured 60 minutes after the hyperbaric exposure. Histopathology of lung tissue was undertaken. RESULTS: Compared with the vehicle alone, BD-AcAc2 prolonged seizure latency in a dose-dependent manner (P < 0.01). The HBO-induced increase in brain malondialdehyde, BLF protein and lung water were significantly reduced by BD-AcAc2 (P < 0.01). CONCLUSION: Oral administration of the ketone ester BD-AcAc2 significantly protected against CNS-OT and concomitant ALI. Alleviation of oxidative stress may be one underlying mechanism providing this effect.


Asunto(s)
Acetoacetatos/uso terapéutico , Lesión Pulmonar Aguda , Encéfalo/efectos de los fármacos , Butileno Glicoles/uso terapéutico , Oxigenoterapia Hiperbárica , Acetoacetatos/farmacología , Lesión Pulmonar Aguda/tratamiento farmacológico , Animales , Oxigenoterapia Hiperbárica/efectos adversos , Ratones , Oxígeno , Ratas Sprague-Dawley , Convulsiones/tratamiento farmacológico
4.
Cell Physiol Biochem ; 47(5): 1800-1808, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29953977

RESUMEN

BACKGROUND/AIMS: Reactive oxygen species (ROS) are considered fundamental in various physiological/pathophysiological processes and prevention/treatment measures such as hyperbaric oxygen (HBO) therapy. In this study, the origination of ROS in human umbilical vein endothelial cells was investigated under basal and HBO conditions. METHODS: Whole cell or mitochondria-targeted fluorescent probes were applied to mark superoxide anion (O2-), and the ROS produced from mitochondrial respiratory chain (MRC), NADPH oxidase (NOX) and xanthine oxidase (XO) were identified by flow cytometry, confocal imaging and microplate fluorometry with or without specific inhibitors. An algorithm was established to calculate ROS proportion of each source. RESULTS: HBO increased ROS to about 2.14-2.44 fold in mitochondria and 1.32-1.42 fold in whole cell. Then ROS levels were significantly decreased by MRC inhibition about 30% and 16%, respectively. NOX or XO inhibition did not affect HBO-induced ROS generation. Based on these data, it could be further estimated that mitochondrial ROS accounted for 32%-39% of basal whole-cell ROS including 3% from MRC complex II, and NOX accounted for at least 24%-29%. Following HBO treatment, almost all increased ROS originated from mitochondria, and MRC complex II contributed at least 45%-60%. CONCLUSION: This study provided a simple but effective method to estimate the origination of intracellular ROS and found that MRC were the main source of HBO-induced ROS generation.


Asunto(s)
Células Endoteliales de la Vena Umbilical Humana/metabolismo , Oxigenoterapia Hiperbárica , Oxígeno/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Transporte de Electrón , Humanos , Mitocondrias/metabolismo , Oxígeno/farmacología , Especies Reactivas de Oxígeno/análisis
5.
Exp Biol Med (Maywood) ; 243(9): 770-779, 2018 05.
Artículo en Inglés | MEDLINE | ID: mdl-29763367

RESUMEN

During diving, central nervous system oxygen toxicity may cause drowning or barotrauma, which has dramatically limited the working benefits of hyperbaric oxygen in underwater operations and clinical applications. The aim of this study is to understand the effects and the underlying mechanism of heat shock protein 70 on central nervous system oxygen toxicity and its mechanisms in vivo and in vitro. Rats were given geranylgeranylacetone (800 mg/kg) orally to induce hippocampal expression of heat shock protein 70 and then treated with hyperbaric oxygen. The time course of hippocampal heat shock protein 70 expression after geranylgeranylacetone administration was measured. Seizure latency and first electrical discharge were recorded to evaluate the effects of HSP70 on central nervous system oxygen toxicity. Effects of inhibitors of nitric oxide synthase and nuclear factor-κB on the seizure latencies and changes in nitric oxide, nitric oxide synthase, and nuclear factor-κB levels in the hippocampus tissues were examined. In cell experiments, hippocampal neurons were transfected with a virus vector carrying the heat shock protein 70 gene (H3445) before hyperbaric oxygen treatment. Cell viability, heat shock protein 70 expression, nitric oxide, nitric oxide synthase, and NF-κB levels in neurons were measured. The results showed that heat shock protein 70 expression significantly increased and peaked at 48 h after geranylgeranylacetone was given. Geranylgeranylacetone prolonged the first electrical discharge and seizure latencies, which was reversed by neuronal nitric oxide synthase, inducible nitric oxide synthase and NF-κB inhibitors. Nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels in the hippocampus were significantly increased after hyperbaric oxygen exposure, but reversed by geranylgeranylacetone, while heat shock protein 70 inhibitor quercetin could inhibit this effect of geranylgeranylacetone. In the in vitro study, heat shock protein 70-overexpression decreased the nitric oxide, nitric oxide synthase, and inducible nitric oxide synthase levels as well as the cytoplasm/nucleus ratio of nuclear factor-κB and protected neurons from hyperbaric oxygen-induced cell injury. In conclusion, overexpression of heat shock protein 70 in hippocampal neurons may protect rats from central nervous system oxygen toxicity by suppression of neuronal nitric oxide synthase and inducible nitric oxide synthase-mediated nitric oxide production and translocation of nuclear factor-κB to nucleus. Impact statement Because the pathogenesis of central nervous system oxygen toxicity (CNS-OT) remains unclear, there are few interventions available. To develop an efficient strategy against CNS-OT, it is necessary to understand its pathogenesis and in particular, the relevant key factors involved. This study examined the protective effects of heat shock protein 70 (HSP70) on CNS-OT via in vivo and in vitro experiments. Our results indicated that overexpression of HSP70 in hippocampal neurons may protect rats from CNS-OT by suppression of nNOS and iNOS-mediated NO production and the activation of NF-κB. These findings contribute to clarification of the role of HSP70 in CNS-OT and provide us a potential novel target to prevent CNS-OT. Clarification of the involvement of NO, NOS and NF-κB provides new insights into the mechanism of CNS-OT and may help us to develop new approach against it by interfering these molecules.


Asunto(s)
Proteínas HSP70 de Choque Térmico/metabolismo , Hipocampo/metabolismo , FN-kappa B/metabolismo , Neuronas/metabolismo , Óxido Nítrico/metabolismo , Oxígeno/toxicidad , Animales , Hipocampo/patología , Oxigenoterapia Hiperbárica/efectos adversos , Masculino , Neuronas/patología , Óxido Nítrico Sintasa/metabolismo , Ratas , Ratas Sprague-Dawley
6.
J Exp Biol ; 221(Pt 5)2018 03 07.
Artículo en Inglés | MEDLINE | ID: mdl-29212841

RESUMEN

Decompression sickness (DCS) occurs when ambient pressure is severely reduced during diving and aviation. Hyperbaric oxygen (HBO) pretreatment has been shown to exert beneficial effects on DCS in rats via heat-shock proteins (HSPs). We hypothesized that HBO pretreatment will also reduce DCS via HSPs in swine models. In the first part of our investigation, six swine were subjected to a session of HBO treatment. HSP32, 60, 70 and 90 were detected, before and at 6, 12, 18, 24 and 30 h following exposure in lymphocytes. In the second part of our investigation, another 10 swine were randomly assigned into two groups (five per group). All swine were subjected to two simulated air dives in a hyperbaric chamber with an interval of 7 days. Eighteen hours before each dive, the swine were pretreated with HBO or air: the first group received air pretreatment prior to the first dive and HBO pretreatment prior to the second; the second group were pretreated with HBO first and then air. Bubble loads, skin lesions, inflammation and endothelial markers were detected after each dive. In lymphocytes, all HSPs increased significantly (P<0.05), with the greatest expression appearing at 18 h for HSP32 and 70. HBO pretreatment significantly reduced all the determined changes compared with air pretreatment. The results demonstrate that a single exposure to HBO 18 h prior to diving effectively protects against DCS in the swine model, possibly via induction of HSPs.


Asunto(s)
Enfermedad de Descompresión/prevención & control , Proteínas de Choque Térmico/metabolismo , Oxigenoterapia Hiperbárica , Animales , Enfermedad de Descompresión/sangre , Enfermedad de Descompresión/fisiopatología , Buceo , Linfocitos/metabolismo , Masculino , Sus scrofa
7.
Sci Rep ; 7: 41288, 2017 01 23.
Artículo en Inglés | MEDLINE | ID: mdl-28112272

RESUMEN

Endothelial dysfunction is involved in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin, the main active compound in horse chestnut seed extract, is well known for its endothelial protection and anti-inflammatory properties. This study aimed to investigate the potential protection of escin against DCS in rats. Escin was administered orally to adult male rats for 7 d (1.8 mg/kg/day) before a simulated air dive. After decompression, signs of DCS were monitored, and blood and pulmonary tissue were sampled for the detection of endothelia related indices. The incidence and mortality of DCS were postponed and decreased significantly in rats treated with escin compared with those treated with saline (P < 0.05). Escin significantly ameliorated endothelial dysfunction (increased serum E-selectin and ICAM-1 and lung Wet/Dry ratio, decreased serum NO), and oxidative and inflammatory responses (increased serum MDA, MPO, IL-6 and TNF-α) (P < 0.05 or P < 0.01). The results suggest escin has beneficial effects on DCS related to its endothelia-protective properties and might be a drug candidate for DCS prevention and treatment.


Asunto(s)
Enfermedad de Descompresión/tratamiento farmacológico , Células Endoteliales/metabolismo , Escina/uso terapéutico , Sustancias Protectoras/uso terapéutico , Animales , Antioxidantes/farmacología , Biomarcadores/metabolismo , Enfermedad de Descompresión/sangre , Enfermedad de Descompresión/enzimología , Células Endoteliales/efectos de los fármacos , Células Endoteliales/enzimología , Escina/farmacología , Inflamación/patología , Masculino , Malondialdehído/sangre , Sustancias Protectoras/farmacología , Ratas Sprague-Dawley , Superóxido Dismutasa/metabolismo
8.
Redox Biol ; 10: 108-118, 2016 12.
Artículo en Inglés | MEDLINE | ID: mdl-27721085

RESUMEN

Spinal cord injury (SCI) is a debilitating disease, effective prevention measures are in desperate need. Our previous work found that hyperbaric oxygen (HBO) preconditioning significantly protected rats from SCI after stimulated diving, and in vitro study further testified that HBO protected primary cultured rat spinal neurons from oxidative insult and oxygen glucose deprivation injury via heat shock protein (HSP) 32 induction. In this study, underlying molecular mechanisms were further investigated. The results showed that a single exposure to HBO significantly increased intracellular levels of reactive oxygen species (ROS) and nitric oxide (NO) and activated MEK1/2, ERK1/2, p38 MAPK, CREB, Bach1 and Nrf2. The induction of HSP32 by HBO was significantly reversed by pretreatment neurons with ROS scavenger N-Acetyl-L-cysteine, p38 MAPK inhibitor or Nrf2 gene knockdown, enhanced by MEK1/2 inhibitors or gene knockdown but not by ERK1/2 inhibitor. CREB knockdown did not change the expression of HSP32 induced by HBO. N-Acetyl-L-cysteine significantly inhibited the activation of MEK1/2, ERK1/2, p38 MAPK, and Nrf2. Activation of Nrf2 was significantly inhibited by p38 MAPK inhibitor and the nuclear export of Bach1 was significantly enhanced by MEK1/2 inhibitor. The results demonstrated that HBO induces HSP32 expression through a ROS/p38 MAPK/Nrf2 pathway and the MEK1/2/Bach1 pathway contributes to negative regulation in the process. More importantly, as we know, this is the first study to delineate that ERK1/2 is not the only physiological substrates of MEK1/2.


Asunto(s)
Hemo Oxigenasa (Desciclizante)/metabolismo , Oxigenoterapia Hiperbárica/métodos , Óxido Nítrico/metabolismo , Especies Reactivas de Oxígeno/metabolismo , Médula Espinal/citología , Animales , Factores de Transcripción con Cremalleras de Leucina de Carácter Básico/metabolismo , Células Cultivadas , Femenino , Sistema de Señalización de MAP Quinasas , Factor 2 Relacionado con NF-E2/metabolismo , Neuronas/citología , Neuronas/metabolismo , Fosforilación , Ratas , Ratas Sprague-Dawley , Médula Espinal/metabolismo
9.
Undersea Hyperb Med ; 42(1): 49-56, 2015.
Artículo en Inglés | MEDLINE | ID: mdl-26094304

RESUMEN

This study aimed to investigate the protective effects of pravastatin on hyperbaric hyperoxia-induced lung injury (HILI). C57BL/6 mice were randomly assigned into three groups: control group, HILI group and pravastatin (Pra) group. Mice in the HILI and Pra groups were subjected to exposure to pure oxygen at 2.5 atm abs for six hours. Mice in the Pra group were intraperitoneally treated with pravastatin at 15 mg/kg. immediately after exposure. At 24 hours, the lungs were collected for HE staining, TUNEL staining and detection of lung edema, myeloperoxidase (MPO) activity and cytokines, and bronchoalveolar lavage fluid (BALF) was harvested for cell-counting. Pravastatin treatment significantly improved the pathology of the lung after HILI (reduction in thickness of alveolar septum, attenuation of lung edema, fracturing of alveolar septa and decrease in infiltrated leukocytes); reduced the number of apoptotic cells; inhibited lung MPO activity; and regulated the balance between pro-inflammatory and anti-inflammatory cytokines. Our findings suggest that pravastatin may exert a protective effect on lung injury after hyperbaric hyperoxia exposure by inhibiting inflammation.


Asunto(s)
Lesión Pulmonar Aguda/prevención & control , Inhibidores de Hidroximetilglutaril-CoA Reductasas/farmacología , Oxigenoterapia Hiperbárica/efectos adversos , Hiperoxia/complicaciones , Pravastatina/farmacología , Lesión Pulmonar Aguda/etiología , Lesión Pulmonar Aguda/patología , Animales , Líquido del Lavado Bronquioalveolar/citología , Quimiocina CXCL2/análisis , Etiquetado Corte-Fin in Situ , Interleucina-10/análisis , Interleucina-1beta/análisis , Pulmón/química , Masculino , Ratones , Ratones Endogámicos C57BL , Peroxidasa/análisis , Edema Pulmonar/tratamiento farmacológico
10.
Undersea Hyperb Med ; 41(3): 183-202, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-24984313

RESUMEN

Oxygen therapy is one of the most widely used clinical interventions to counteract insufficient pulmonary oxygen delivery in patients with severe lung injury. However, prolonged exposure to hyperoxia at elevated partial pressure leads to inflammation and acute lung injury. The population at risk for this condition has markedly increased with the advent of efficient systems for delivery of high concentrations of oxygen in hospitals. Thus, the therapy of hyperoxia-induced lung injury has been a focus in studies of pediatrics and pulmonary medicine. In this paper, we briefly summarized the advances in the therapies of hyperoxia-induced lung injury on the basis of its pathogenesis. We hope our summary will help provide evidence for further investigation of therapeutic measures for hyperoxia-induced lung injury.


Asunto(s)
Lesión Pulmonar Aguda/terapia , Oxigenoterapia Hiperbárica/efectos adversos , Modelos Animales , Terapia por Inhalación de Oxígeno/efectos adversos , Lesión Pulmonar Aguda/etiología , Animales , Estrés Oxidativo , Terapia por Inhalación de Oxígeno/métodos , Presión Parcial
11.
J Neurotrauma ; 31(15): 1343-53, 2014 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-24716787

RESUMEN

In this study, we investigated whether nuclear factor erythroid 2-related factor 2 (Nrf2) activation in astrocytes contributes to the neuroprotection induced by a single hyperbaric oxygen preconditioning (HBO-PC) against spinal cord ischemia/reperfusion (SCIR) injury. In vivo: At 24 h after a single HBO-PC at 2.5 atmospheres absolute for 90 min, the male ICR mice underwent SCIR injury by aortic cross-clamping surgery and observed for 48 h. HBO-PC significantly improved hindlimb motor function, reduced secondary spinal cord edema, ameliorated the reactivity of spinal motor-evoked potentials, and slowed down the process of apoptosis to exert neuroprotective effects against SCIR injury. At 12 h or 24 h after HBO-PC without aortic cross-clamping surgery, Western blot, enzyme-linked immunosorbent assay, realtime-polymerase chain reaction and double-immunofluorescence staining were used to detect the Nrf2 activity of spinal cord tissue, such as mRNA level, protein content, DNA binding activity, and the expression of downstream gene, such as glutamate-cysteine ligase, γ-glutamyltransferase, multidrug resistance protein 1, which are key proteins for intracellular glutathione synthesis and transit. The Nrf2 activity and downstream genes expression were all enhanced in normal spinal cord with HBO-PC. Glutathione content of spinal cord tissue with HBO-PC significantly increased at all time points after SCIR injury. Moreover, Nrf2 overexpression mainly occurs in astrocytes. In vitro: At 24 h after HBO-PC, the primary spinal astrocyte-neuron co-cultures from ICR mouse pups were subjected to oxygen-glucose deprivation (OGD) for 90 min to simulate the ischemia-reperfusion injury. HBO-PC significantly increased the survival rate of neurons and the glutathione content in culture medium, which was mainly released from asctrocytes. Moreover, the Nrf2 activity and downstream genes expression induced by HBO-PC were mainly enhanced in astrocytes, but not in neurons. In conclusion, our findings demonstrated that spinal cord ischemic tolerance induced by HBO-PC may be mainly related to Nrf2 activation in astrocytes.


Asunto(s)
Astrocitos/metabolismo , Oxigenoterapia Hiperbárica/métodos , Precondicionamiento Isquémico/métodos , Factor 2 Relacionado con NF-E2/metabolismo , Animales , Western Blotting , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Técnica del Anticuerpo Fluorescente , Etiquetado Corte-Fin in Situ , Masculino , Ratones , Ratones Endogámicos ICR , Reacción en Cadena en Tiempo Real de la Polimerasa , Recuperación de la Función , Traumatismos de la Médula Espinal/metabolismo , Isquemia de la Médula Espinal/metabolismo
12.
PLoS One ; 9(1): e85967, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-24465817

RESUMEN

OBJECTIVE: Hyperbaric oxygen (HBO) preconditioning (HBO-PC) has been testified to have protective effects on spinal cord injury (SCI). However, the mechanisms remain enigmatic. The present study aimed to explore the effects of HBO-PC on primary rat spinal neurons against oxidative injury and oxygen-glucose deprivation (OGD) and the relationship with heat shock proteins (HSPs). METHODS: Primary rat spinal neurons after 7 days of culture were used in this study. HSPs were detected in rat spinal neurons following a single exposure to HBO at different time points by Western blot. Using lactate dehydrogenase release assay and cell counting kit-8 assay, the injuries induced by hydrogen peroxide (H2O2) insult or OGD were determined and compared among neurons treated with HBO-PC with or without HSP inhibitors. RESULTS: The results of Western blot showed that HSP27, HSP70 and HSP90 have a slight but not significant increase in primary neurons following HBO exposure. However, HSP32 expression significantly increased and reached highest at 12 h following HBO exposure. HBO-PC significantly increased the cell viability and decreased the medium lactate dehydrogenase content in cultures treated with H2O2 or OGD. Pretreatment with zinc protoporphyrin IX, a specific inhibitor of HSP32, significantly blocked the protective effects of HBO-PC. CONCLUSIONS: These results suggest that HBO-PC could protect rat spinal neurons in vitro against oxidative injury and OGD mostly by up-regulating of HSP32 expression.


Asunto(s)
Glucosa/deficiencia , Hemo Oxigenasa (Desciclizante)/metabolismo , Oxigenoterapia Hiperbárica , Neuronas/metabolismo , Estrés Oxidativo/efectos de los fármacos , Oxígeno/farmacología , Columna Vertebral/patología , Regulación hacia Arriba/efectos de los fármacos , Animales , Células Cultivadas , Hipoxia/patología , Neuronas/efectos de los fármacos , Ratas , Traumatismos de la Médula Espinal/metabolismo , Traumatismos de la Médula Espinal/patología , Columna Vertebral/efectos de los fármacos , Factores de Tiempo
13.
Undersea Hyperb Med ; 41(6): 573-8, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25562948

RESUMEN

Hyperbaric oxygen therapy is one of the most widely used clinical interventions to counteract insufficient pulmonary oxygen delivery in patients with severe lung injury. However, prolonged exposure to hyperoxia leads to inflammation and acute lung injury. This study aimed to investigate the protective effect of hydrogen sulfide on hyperbaric hyperoxia-induced lung injury. Rats were intraperitoneally treated with sodium hydrosulphide (NaHS) at 28 µmol/kg immediately before hyperoxia exposure and then exposed to pure oxygen at 2.5 atmospheres absolute (atm abs) with continuous ventilation for six hours, Immediately after hyperoxia exposure, rats were sacrificed via anesthesia. The bronchoalveolar lavage fluid (BALF) was harvested for the detection of protein concentration and IL-1 content, and the lungs were collected for HE staining, TUNEL staining and detection of wet/dry weight ratio. Our results showed hyperbaric hyperoixa exposure could significantly damage the lung (HE staining), increase the protein and IL-13 in the BALF, elevate the wet/dry Weight ratio and raise the TUNEL positive cells. However, pre-treatment with hydrogen sulfide improved the lung morphology, reduced the TUNEL positive cells and attenuated the lung inflammation (reduction in IL-13 of BALF and HE staining). Taken together, our findings indicate that hydrogen sulfide pretreatment may exert protective effects on hyperbaric hyperoxia-induced lung injury.


Asunto(s)
Lesión Pulmonar Aguda/prevención & control , Gasotransmisores/uso terapéutico , Sulfuro de Hidrógeno/uso terapéutico , Oxigenoterapia Hiperbárica/efectos adversos , Lesión Pulmonar Aguda/etiología , Animales , Antracenos , Líquido del Lavado Bronquioalveolar/química , Etiquetado Corte-Fin in Situ , Inyecciones Intraperitoneales , Interleucina-1beta/análisis , Pulmón/efectos de los fármacos , Pulmón/patología , Masculino , Proteínas/análisis , Ratas Sprague-Dawley , Sulfuros/farmacología
14.
Exp Biol Med (Maywood) ; 238(1): 12-22, 2013 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-23479759

RESUMEN

Decompression sickness (DCS) is a major concern in diving and space walk. Hyperbaric oxygen (HBO) preconditioning has been proved to enhance tolerance to DCS via nitric oxide. Heat-shock protein (HSP) 70 was also found to have protective effects against DCS. We hypothesized that the beneficial effects of HBO preconditioning on DCS was related to levels of elevated HSP70. HSPs (70, 27 and 90) expressed in tissues of spinal cord and lung in rats was detected at different time points following HBO exposure by Western blot. HSP27 and HSP90 showed a slight but not significant increase after HBO. HSP70 increased and reached highest at 18 h following exposure before decreasing. Then rats were exposed to HBO and subjected to simulated air dive and rapid decompression to induce DCS 18 h after HBO. The severity of DCS, along with levels of HSP70 expression, as well as the extent of oxidative and apoptotic parameters in the lung and spinal cord were compared among different groups of rats pretreated with HBO, HBO plus NG-nitro-l-arginine-methyl ester (l-NAME), HBO plus quercetin or normobaric air. HBO preconditioning significantly reduced the morbidity of DCS (from 66.7% to 36.7%), reduced levels of oxidation (malondialdehyde, 8-hydroxyguanine and hydrogen peroxide) and apoptosis (caspase-3 and -9 activities and the number of apoptotic cells). l-NAME or quercetin eliminated most of the beneficial effects of HBO on DCS, and counteracted the stimulation of HSP70 by HBO. Bubbles in pulmonary artery were detected using ultrasound imaging to observe the possible effect of HBO preconditioning on DCS bubble formation. The amounts of bubbles in rats pretreated with HBO or air showed no difference. These results suggest that HSP70 was involved in the beneficial effects of HBO on DCS in rats, suspected be by the antioxidation and antiapoptosis effects.


Asunto(s)
Enfermedad de Descompresión/patología , Enfermedad de Descompresión/fisiopatología , Proteínas HSP70 de Choque Térmico/metabolismo , Oxigenoterapia Hiperbárica , Animales , Western Blotting , Perfilación de la Expresión Génica , Pulmón/química , Pulmón/patología , Masculino , Ratas , Ratas Sprague-Dawley , Índice de Severidad de la Enfermedad , Médula Espinal/química , Médula Espinal/patología
15.
PLoS One ; 7(11): e50079, 2012.
Artículo en Inglés | MEDLINE | ID: mdl-23185538

RESUMEN

BACKGROUND: Decompression illness (DCI) is a major concern in pressure-related activities. Due to its specific prerequisite conditions, DCI is rare in comparison with other illnesses and most physicians are inexperienced in treatment. In a fishery area in northern China, during the past decade, tens of thousands of divers engaged in seafood harvesting and thousands suffered from DCI. We established a hyperbaric facility there and treated the majority of the cases. METHODS AND RESULTS: A total of 5,278 DCI cases were admitted in our facility from February 2000 through December 2010 and treated using our recompression schedules. Cutaneous abnormalities, joint and muscular pain and neurological manifestations were three most common symptoms. The initial symptom occurred within 6 h after surfacing in 98.9% of cases, with an overall median latency of 62 min. The shorter the latent time, the more serious the symptoms would be (P<0.0001). Nine cases died before recompression and 5,269 were treated using four recompression schedules, with an overall effectiveness rate of 99.3%. The full recovery rate decreased with the increase of the delay from the onset of symptoms to the treatment (P<0.0001). CONCLUSIONS: DCI presents specific occurrence rules. Recompression should be administered as soon as possible and should never be abandoned irrespective of the delay. The recompression schedules used were effective and flexible for variety conditions of DCI.


Asunto(s)
Enfermedad de Descompresión/terapia , Oxigenoterapia Hiperbárica , Recuperación de la Función , Adolescente , Adulto , Enfermedad de Descompresión/diagnóstico , Enfermedad de Descompresión/etiología , Enfermedad de Descompresión/mortalidad , Buceo/efectos adversos , Humanos , Masculino , Persona de Mediana Edad , Índice de Severidad de la Enfermedad , Tasa de Supervivencia , Factores de Tiempo , Resultado del Tratamiento
17.
Undersea Hyperb Med ; 37(3): 173-80, 2010.
Artículo en Inglés | MEDLINE | ID: mdl-20568547

RESUMEN

Divers are at risk of decompression sickness (DCS) when the ambient pressure decrease exceeds a critical threshold. Hyperbaric oxygen (HBO2) preconditioning has been used to prevent various injuries, but the protective effect on DCS has not been well explored. To investigate the prophylactic effect of HBO2 on DCS, rats were pretreated with HBO2 (250 kPa-60 minutes) (all the pressures described here are absolute pressure) for 18 hours before a simulated air dive (700 kPa-100 minutes) with fast decompression to the surface at the rate of 200 kPa/min (n=33). During the following 30 minutes, the rats walked in a 3 m/minute rotating cage and were monitored for signs of DCS. The control rats were pretreated with normobaric air (n=30), normoxic hyperbaric nitrox (250 kPa, 8.4% O2) (n=13), or N(G)-nitro-L-arginine methyl ester (L-NAME) 30 minutes before HBO2 exposure (n=13). Nitric oxide (NO) levels were recorded immediately and 18 hours after HBO2 exposure in the brain and spinal cord. The incidence of DCS in rats pretreated with HBO2 was 30.3%, which was significantly lower than those treated with normobaric air (63.3%) (p<0.05) or hyperbaric nitrox (61.5%) (p<0.05). The onset time of DCS of the rats pretreated with HBO2 was significantly delayed compared with those treated with air (p<0.05). L-NAME nullified the HBO2 preconditioning effect. HBO2 increased NO level in the rat brain and spinal cord right after exposure; this effect was inhibited by L-NAME. Taken together, HBO2 preconditioning reduced the incidence of DCS in rats, and NO was involved in the prophylactic effect.


Asunto(s)
Enfermedad de Descompresión/prevención & control , Oxigenoterapia Hiperbárica/métodos , Óxido Nítrico/metabolismo , Animales , Encéfalo/metabolismo , Enfermedad de Descompresión/metabolismo , Inhibidores Enzimáticos/administración & dosificación , Masculino , Actividad Motora/fisiología , NG-Nitroarginina Metil Éster/administración & dosificación , Óxido Nítrico/análisis , Nitrógeno/administración & dosificación , Oxígeno/administración & dosificación , Ratas , Ratas Sprague-Dawley , Médula Espinal/metabolismo , Factores de Tiempo
18.
J Neurotrauma ; 26(1): 55-66, 2009 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-19196076

RESUMEN

This study tested the hypothesis that spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is mediated by inhibition of early apoptosis. Male Sprague-Dawley rats were preconditioned with consecutive 4 cycles of 1-h HBO exposures (2.5 atmospheres absolute [ATA], 100% O(2)) at a 12-h interval. At 24 h after the last HBO pretreatment, rats underwent 9 min of spinal cord ischemia induced by occlusion of the descending thoracic aorta in combination with systemic hypotension (40 mmHg). Spinal cord ischemia produced marked neuronal death and neurological dysfunction in animals. HBO-PC enhanced activities of Mn-superoxide dismutase (Mn-SOD) and catalase, as well as the expression of Bcl-2 in the mitochondria in the normal spinal cord at 24 h after the last pretreatment (before spinal cord ischemia), and retained higher levels throughout the early reperfusion in the ischemic spinal cord. In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated. HBO-PC improved neurobehavioral scores and reduced neuronal apoptosis in the anterior, intermediate, and dorsal gray matter of lumbar segment at 24 h after spinal cord ischemia. HBO-PC increased nitric oxide (NO) production. L-nitroarginine-methyl-ester (L-NAME; 10 mg/kg), a nonselective NO synthase (NOS) inhibitor, applied before each HBO-PC protocol abolished these beneficial effects of HBO-PC. We conclude that HBO-PC reduced spinal cord ischemia-reperfusion injury by increasing Mn-SOD, catalase, and Bcl-2, and by suppressing mitochondrial apoptosis pathway. NO may be involved in this neuroprotection.


Asunto(s)
Apoptosis/fisiología , Oxigenoterapia Hiperbárica/métodos , Precondicionamiento Isquémico/métodos , Isquemia de la Médula Espinal/terapia , Animales , Modelos Animales de Enfermedad , Metabolismo Energético/fisiología , Masculino , Mitocondrias/metabolismo , Enfermedades Mitocondriales/etiología , Enfermedades Mitocondriales/fisiopatología , Enfermedades Mitocondriales/terapia , Degeneración Nerviosa/fisiopatología , Degeneración Nerviosa/prevención & control , Degeneración Nerviosa/terapia , Estrés Oxidativo/fisiología , Ratas , Ratas Sprague-Dawley , Recuperación de la Función , Isquemia de la Médula Espinal/metabolismo , Isquemia de la Médula Espinal/fisiopatología , Factores de Tiempo , Resultado del Tratamiento
19.
Life Sci ; 83(7-8): 236-41, 2008 Aug 15.
Artículo en Inglés | MEDLINE | ID: mdl-18644387

RESUMEN

Hyperbaric oxygen preconditioning (HBO-PC) increases the level of HIF-1alpha (hypoxia inducible factor-1alpha) and its target gene VEGF (vascular endothelial growth factor) which is involved in angiogenesis. Liver regeneration is an angiogenesis-dependent process. We hypothesized that HIF-1alpha and VEGF mediated the angiogenesis effect of HBO-PC on regenerating rat liver. Male Sprague Dawley rats received HBO-PC followed by 70% partial hepatectomy. Proliferation of hepatocytes and endothelial cells was evaluated by BrdU (bromodeoxyuridine) staining. Microvascular density was assessed by immunohistochemistry. mRNA expression of HIF-1alpha was assessed by quantitative RT-PCR and protein levels of HIF-1alpha and VEGF were assessed by western blot. HIF-1alpha DNA-binding activity was determined with an ELISA-based kit. HBO-PC increased the proliferation index of endothelial cells and microvascular density at 48 h after partial hepatectomy. The protein level and DNA-binding activity of HIF-1alpha and the protein level of VEGF were increased by HBO-PC before and after partial hepatectomy. Partial hepatectomy alone also increased proliferation index and the expressions of HIF-1alpha and VEGF. Our results indicated that the angiogenesis effect of HBO-PC on liver after partial hepatectomy could be achieved by increased HIF-1alpha activity and VEGF expression. However, the angiogenic effect of HBO-PC is moderate and HBO-PC failed to produce additional effect on the enhancement of HIF-1alpha and VEGF induced by partial hepatectomy alone.


Asunto(s)
Hepatectomía , Oxigenoterapia Hiperbárica , Subunidad alfa del Factor 1 Inducible por Hipoxia/biosíntesis , Regeneración Hepática/efectos de los fármacos , Neovascularización Fisiológica/efectos de los fármacos , Oxígeno/farmacología , Factor A de Crecimiento Endotelial Vascular/biosíntesis , Animales , Proliferación Celular/efectos de los fármacos , Células Endoteliales/metabolismo , Regulación de la Expresión Génica/efectos de los fármacos , Hepatocitos/metabolismo , Inmunohistoquímica/métodos , Masculino , ARN Mensajero/biosíntesis , Ratas , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/métodos
20.
Brain Res ; 1210: 223-9, 2008 May 19.
Artículo en Inglés | MEDLINE | ID: mdl-18407255

RESUMEN

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.


Asunto(s)
Antioxidantes/metabolismo , Isquemia Encefálica/enzimología , Oxigenoterapia Hiperbárica , Precondicionamiento Isquémico , Estrés Oxidativo , Daño por Reperfusión/enzimología , Animales , Encéfalo/enzimología , Isquemia Encefálica/terapia , Catalasa/metabolismo , Activación Enzimática , Enzimas/metabolismo , Glutatión/metabolismo , Infarto de la Arteria Cerebral Media/enzimología , Infarto de la Arteria Cerebral Media/terapia , Masculino , Malondialdehído/metabolismo , Oxígeno/metabolismo , Oxígeno/farmacología , Oxígeno/uso terapéutico , Consumo de Oxígeno/fisiología , Ratas , Ratas Sprague-Dawley , Especies Reactivas de Oxígeno/metabolismo , Daño por Reperfusión/terapia , Superóxido Dismutasa/metabolismo , Superóxido Dismutasa-1 , Regulación hacia Arriba
SELECCIÓN DE REFERENCIAS
DETALLE DE LA BÚSQUEDA