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1.
Asia Pac J Clin Oncol ; 16(2): e3-e11, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31970936

RESUMO

Cancer is a key cause of death worldwide. Despite the development of radiotherapy, chemotherapy and even immunotherapy, surgery remains the standard treatment for cancer patients. Recently, many studies have shown that propofol, a commonly used anesthetic drug, can affect the prognosis of cancer. In this review, we provide an overview of the molecular mechanisms of propofol in the development of cancer. Propofol not only affects epigenetic pathways, such as those involving miRNA, lncRNA and histone acetylation, but also modulates genetic signaling pathways, including the hypoxia, NF-κB, MAPK, SLUG and Nrf2 pathways. In addition, propofol influences the immune function of patients and impacts the degree of immunosuppression. Furthermore, we briefly summarize the clinical trials on the effect of propofol in cancer development. Ultimately, further studies distinguishing the types of tumors in clinical trials are needed to clarify the correlation between propofol and cancer.

2.
Anticancer Drugs ; 31(1): 27-34, 2020 01.
Artigo em Inglês | MEDLINE | ID: mdl-31490283

RESUMO

Ferroptosis is a newly discovered type of cell death decided by iron-dependent lipid peroxidation, but its role in glioblastoma cell death remains unclear. Ibuprofen, a nonsteroidal anti-inflammatory drug (NSAID), has been associated with antitumorigenic effects in many cancers. In this study, we first found that ibuprofen inhibited the viabilities of glioblastoma cells in vitro and in vivo, accompanied by abnormal increase in intracellular lipid peroxidation. Further study showed that the cell growth inhibition caused by ibuprofen could be rescued by the ferroptosis inhibitors deferoxamine (DFO), ferrostatin-1 and Liproxstatin-1. Nuclear factor erythroid 2-related factor 2 (Nrf2), glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) are key regulators of ferroptosis. Our data showed that Nrf2, GPX4 and SLC7A11 were downregulated in glioblastoma cells under ibuprofen treatment. Interestingly, we found that decreased mRNA expression of GPX4 and SLC7A11 was accompanied with reduced Nrf2, which is a redox sensitive transcription factor that controls the expression of intracellular redox-balancing proteins such as GPX4 and SLC7A11. All the data suggested that Nrf2 could regulate the expression of GPX4 and SLC7A11 in glioma cells. Taken together, our findings reveal that ibuprofen could induce ferroptosis of glioblastoma cells via downregulation of Nrf2 signaling pathway and is a potential drug for glioma treatment.

3.
Oncol Lett ; 18(3): 2771-2776, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31452755

RESUMO

Cervical cancer is one of the leading causes of cancer-associated mortality among females; however, the underlying molecular mechanisms of its carcinogenesis remain largely unclear. Previous comprehensive genomic studies have revealed prevalent estrogen receptor 1 (ESR1) mutations in breast cancer, which are rare in certain other types of cancer. To the best of our knowledge, it is unknown whether ESR1 mutations also exist in cervical cancer. Considering the evidence that cervical cancer shares certain genetic aberrations with breast cancer, and that the progression of both breast and cervical cancers can be affected by estrogen, it is possible that cervical cancer may also harbor ESR1 mutations. In the present study, a total of 260 Chinese cervical cancer samples with distinct subtypes were tested for the presence of ESR1 mutations. A total of three heterozygous missense ESR1 mutations, p.K303R (c.908A>G), p.T311M (c.932C>T) and p.Y537C (c.1610A>G), were identified in 3/207 (1.4%) cervical squamous cell carcinoma samples, which were absent in 27 adenosquamous carcinomas and 26 adenocarcinomas samples. Of the three individuals with an ESR1mutation, 1 patient was also diagnosed with ovarian endometriosis and the other 2 patients were diagnosed with a uterine fibroid. A bioinformatics analysis suggested that these ESR1 mutations may be pathogenic by promoting the development of cervical cancer. Furthermore, a previous comprehensive study confirmed that individuals with cervical squamous cell carcinoma possessed ESR1 mutations. These combined studies indicate that ESR1 mutations may participate in the carcinogenesis of cervical squamous cell carcinoma, albeit at a low frequency. In conclusion, the present study identified three potentially pathogenic ESR1 mutations in Chinese cervical squamous cell carcinoma samples, but not in other subtypes.

4.
Environ Toxicol Pharmacol ; 67: 117-123, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30818178

RESUMO

This study was designed to investigate the neuroprotective effect of hyperoxygenate hydrogen-rich saline (HOHS) against brain injury induced by carbon monoxide (CO) poisoning in rats. A rat model of CO poisoning was established by administering CO via intraperitoneal injection to male Sprague-Dawley rats. Forty-eight adult male rats were randomly divided into the following groups: normal control group (NG), CO poisoning group (CO), HOS treatment group (hyperoxygenated solution, HOS) and HOHS treatment group (HOHS). After CO poisoning, the carboxyhemoglobin (COHb) contents in the blood of rats in all the CO poisoning groups were increased significantly. However, HOS and HOHS significantly decreased COHb contents, furthermore, the HOHS group had lower COHb contents than the HOS group. Arterial oxygen partial pressure (PaO2) and arterial oxygen saturation (SaO2) results showed that HOS and HOHS could improve the oxygenation of the rats with CO poisoning. Compared with the CO group, the HOS group and the HOHS group had persistently neuroprotective effect on CO-induced brain injury, as assessed by modified neurological severity score (mNSS), furthermore, the HOHS group had better neurological functional recovery than the HOS group. The neuronal apoptosis induced by CO was also evaluated. Except the NG group, all the CO-poisoning groups had varying degrees of neuronal apoptosis. There was lesser degree of neuronal apoptosis in both the HOS group and the HOHS group than that in the CO group. Moreover, the HOHS group had more minor degree of neuronal apoptosis than the HOS group. Compared with the CO group, the free radicals production in the HOS group and the HOHS group were significantly inhibited. In addition, there were significantly difference in the free radicals production between the HOS group and the HOHS group. We could conclude that HOHS exerted a stronger neuroprotective effect against CO-induced brain injury than HOS, and the neuroprotective mechanism of HOHS may be related with inhibition of both neuronal apoptosis and free radicals.


Assuntos
Lesões Encefálicas/tratamento farmacológico , Intoxicação por Monóxido de Carbono/tratamento farmacológico , Fármacos Neuroprotetores/uso terapêutico , Solução Salina/uso terapêutico , Soluções/uso terapêutico , Animais , Apoptose/efeitos dos fármacos , Lesões Encefálicas/etiologia , Lesões Encefálicas/metabolismo , Intoxicação por Monóxido de Carbono/complicações , Intoxicação por Monóxido de Carbono/metabolismo , Carboxihemoglobina/análise , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Masculino , Neurônios/efeitos dos fármacos , Ratos Sprague-Dawley
5.
J Surg Res ; 239: 103-114, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-30825755

RESUMO

BACKGROUND: Hemorrhagic shock could induce acute lung injury (ALI), which is associated with cell hypoxia, lung tissue inflammation, free radical damage, and excessive cell apoptosis. Our previous studies demonstrated that hyperoxygenated solution could alleviate cell hypoxia. Furthermore, hydrogen-rich solution (HS) could relieve lung tissue inflammation, free radical damage and excessive cell apoptosis. Therefore we hypothesize that Hyperoxygenated Hydrogen-rich solution (HOHS) can protect the lung against ALI. MATERIALS AND METHODS: SD rats were randomly divided into five groups (n = 6 at each time point in each group) and were exposed to Hemorrhagic shock induced ALI, and then treated with lactated Ringer's solution (LRS), hyperoxygenated solution, HS, and HOHS, respectively. The protective effects of these solutions were assessed using methods as follows: arterial blood samples were collected for blood gas analysis; Bronchoalveolar lavage fluid was collected for cell count and protein quantification; lung tissue samples were collected to measure wet/dry ratio, as well as levels of T-SOD, MDA, TNF-α, and IL-6; Caspase-3 and TUNEL-positive cells, and pathological changes were observed under light microscope; ALI was scored using the Smith scoring method; ultrastructural changes of lung tissues were further observed with transmission electron microscopy. RESULTS: The results indicated that PaO2, PaCO2, and T-SOD increased in the three treatment groups (P < 0.05), most significantly in the HOHS group (P < 0.01) compared with the LRS group; and conversely that the levels of lactate, MDA, TNF-α and IL-6, cell count, protein content, caspase-3 and TUNEL-positive cells as well as ALI score decreased in the three treatment groups (P < 0.05), most significantly in the HOHS group (P < 0.01) compared with the LRS group. Morphological observation with optical microscope and electron microscopy showed that compared with the LRS group, cell damage in the three treatment groups improved to a varying extent, especially evident in the HOHS group. CONCLUSIONS: These findings demonstrate that HOHS can protect the lung against ALI induced by hemorrhagic shock.


Assuntos
Lesão Pulmonar Aguda/tratamento farmacológico , Hidratação/métodos , Ressuscitação/métodos , Choque Hemorrágico/complicações , Soluções/administração & dosagem , Lesão Pulmonar Aguda/etiologia , Lesão Pulmonar Aguda/patologia , Administração Oral , Animais , Modelos Animais de Doenças , Humanos , Pulmão/efeitos dos fármacos , Pulmão/patologia , Pulmão/ultraestrutura , Masculino , Microscopia Eletrônica de Transmissão , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Resultado do Tratamento
6.
Front Cell Neurosci ; 12: 289, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30233327

RESUMO

Whether persons with schizophrenia have a higher or lower incidence of cancer has been discussed for a long time. Due to the complex mechanisms and characteristics of different types of cancer, it is difficult to evaluate the exact relationship between cancers and schizophrenia without considering the type of tumor. Schizophrenia, a disabling mental illness that is now recognized as a neurodevelopmental disorder, is more correlated with brain tumors, such as glioma, than other types of tumors. Thus, we mainly focused on the relationship between schizophrenia and glioma morbidity. Glioma tumorigenesis and schizophrenia may share similar mechanisms; gene/pathway disruption would affect neurodevelopment and reduce the risk of glioma. The molecular defects of disrupted-in-schizophrenia-1 (DISC1), P53, brain-derived neurotrophic factor (BDNF) and C-X-C chemokine receptors type 4 (CXCR4) involved in schizophrenia pathogenesis might play opposite roles in glioma development. Many microRNAs (miRNAs) such as miR-183, miR-9, miR-137 and miR-126 expression change may be involved in the cross talk between glioma prevalence and schizophrenia. Finally, antipsychotic drugs may have antitumor effects. All these factors show that persons with schizophrenia have a decreased incidence of glioma; therefore, epidemiological investigation and studies comparing genetic and epigenetic aberrations involved in both of these complex diseases should be performed. These studies can provide more insightful knowledge about glioma and schizophrenia pathophysiology and help to determine the target/strategies for the prevention and treatment of the two diseases.

7.
J Dent Anesth Pain Med ; 18(1): 1-8, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29556553

RESUMO

In recent years, with continuous research efforts targeted at studying the effects of pre- and after-treatment of inhaled anesthetics, significant progress has been made regarding the common clinical use of low concentrations of inhaled sevoflurane and its effect on induced central ischemia tolerance by pre- and post-treatment. In this study, we collected, analyzed, classified, and summarized recent literature regarding the effect of sevoflurane on central ischemia tolerance and its related mechanisms. In addition, we provide a theoretical basis for the clinical application of sevoflurane to protect the central nervous system and other important organs against ischemic injury.

8.
Mol Neurobiol ; 55(1): 652-667, 2018 01.
Artigo em Inglês | MEDLINE | ID: mdl-27987133

RESUMO

Paired immunoglobulin-like receptor B (PirB) has been identified as a new receptor for myelin-associated inhibitory (MAI) proteins, which may play important role in axonal regeneration and corticospinal tract (CST) projection associated with neurobehavioral function recovery after stroke. Here, we found that the expression of PirB was increased in the cortical penumbra from 1 to 28 days after transient focal cerebral ischemic reperfusion of rats. Then, transactivator of transcription-PirB extracellular peptide (TAT-PEP) was generated that might block the interactions between MAIs and PirB. The results showed that TAT-PEP displayed high affinity for MAIs and ameliorated their inhibitory effect on neurite growth. Furthermore, TAT-PEP can widely distribute in the penumbra after intraperitoneal injection. Then, we found that TAT-PEP enhanced neurite growth and alleviated growth cone collapse after oxygen glucose deprivation (OGD) injury. In addition, TAT-PEP promoted long-term neurobehavioral functional recovery through enhancing axonal regeneration and CST projection. Finally, the observations demonstrated that POSH/RhoA/growth-associated protein 43 (GAP43) as PirB-associated downstream signaling molecules played important role in neurobehavioral functional recovery after stroke. Moreover, the underlying mechanism associated with TAT-PEP-mediated promoting axonal regeneration and CST projection was by intervening in the expression of POSH, RhoA, and GAP43. These studies suggest that TAT-PEP may represent an attractive therapeutic strategy against stroke.


Assuntos
Axônios/metabolismo , Regeneração Nervosa , Tratos Piramidais/patologia , Receptores Imunológicos/metabolismo , Proteínas Recombinantes de Fusão/farmacologia , Recuperação de Função Fisiológica , Acidente Vascular Cerebral/fisiopatologia , Produtos do Gene tat do Vírus da Imunodeficiência Humana/farmacologia , Animais , Comportamento Animal , Isquemia Encefálica/patologia , Glucose/deficiência , Cones de Crescimento/metabolismo , Masculino , Regeneração Nervosa/efeitos dos fármacos , Neuritos/efeitos dos fármacos , Neuritos/metabolismo , Oxigênio , Peptídeos/farmacologia , Tratos Piramidais/efeitos dos fármacos , Tratos Piramidais/fisiopatologia , Ratos Sprague-Dawley , Recuperação de Função Fisiológica/efeitos dos fármacos , Transdução de Sinais , Acidente Vascular Cerebral/patologia
9.
J Surg Res ; 220: 363-371, 2017 12.
Artigo em Inglês | MEDLINE | ID: mdl-29180204

RESUMO

BACKGROUND: It is not known whether simultaneous delivery of hydrogen and oxygen can reduce injury caused by hemorrhagic shock and resuscitation (HSR). This study investigated the therapeutic potential of hyperoxygenated hydrogen-rich solution (HHOS), a combined hydrogen/oxygen carrier, in a rat model of HSR-induced liver injury. MATERIALS AND METHODS: Rats (n = 60) were randomly divided into 5 groups (n = 6 per group at each time point). One group underwent sham operation, and the others were subjected to severe hemorrhagic shock and then treated with lactated Ringer's solution (LRS), hydrogen-rich solution, hyperoxygenated solution, or HHOS. At 2 and 6 h after resuscitation, blood samples (n = 6) were collected from the femoral artery and serum concentrations of alanine aminotransferase and aspartate aminotransferase (AST) were measured. Rats were then sacrificed, and histopathological changes in the liver were evaluated by quantifying the percentage of apoptotic cells by caspase-3 immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick-end labeling. Inflammation was assessed by assessing malondialdehyde content and tumor necrosis factor-α, and interleukin (IL)-6 expression. RESULTS: Compared to lactated Ringer's solution, hydrogen-rich solution, or hyperoxygenated solution groups, serum AST and alanine aminotransferase levels and IL-6, tumor necrosis factor-α, and malondialdehyde expression in liver tissue were decreased by HHOS treatment. The number of caspase-3- and terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells was decreased (P < 0.05) by HHOS treatment, 2 and 6 h after resuscitation. CONCLUSIONS: HHOS has protective effects against liver injury in a rat model of HSR.


Assuntos
Insuficiência Hepática/prevenção & controle , Ressuscitação/efeitos adversos , Choque Hemorrágico/complicações , Soluções/uso terapêutico , Animais , Citocinas/metabolismo , Modelos Animais de Doenças , Insuficiência Hepática/etiologia , Insuficiência Hepática/patologia , Hidrogênio/uso terapêutico , Fígado/metabolismo , Fígado/ultraestrutura , Masculino , Oxigênio/uso terapêutico , Distribuição Aleatória , Ratos Sprague-Dawley
10.
J Dent Anesth Pain Med ; 17(1): 13-20, 2017 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-28879324

RESUMO

Cleft palate is one of the most common congenital malformations of the oral and maxillofacial region, with an incidence rate of around 0.1%. Early surgical repair is the only method for treatment of a cleft lip and palate. However, because of the use of inhalation anesthesia in children and the physiological characteristics of the cleft palate itself combined with the particularities of cleft palate surgery, the incidence rate of postoperative emergence agitation (EA) in cleft palate surgery is significantly higher than in other types of interventions. The exact mechanism of EA is still unclear. Although restlessness after general anesthesia in children with cleft palate is self-limiting, its effects should be considered by clinicians. In this paper, the related literature on restlessness after surgery involving general anesthesia in recent years is summarized. This paper focuses on induction factors as well as prevention and treatment of postoperative restlessness in children with cleft palate after general anesthesia. The corresponding countermeasures to guide clinical practice are also presented in this paper.

11.
Front Immunol ; 8: 774, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28729866

RESUMO

Cytokine-induced killer (CIK) cells are a heterogeneous population of effector CD3+CD56+ natural killer T cells, which can be easily expanded in vitro from peripheral blood mononuclear cells. CIK cells work as pharmacological tools for cancer immunotherapy as they exhibit MHC-unrestricted, safe, and effective antitumor activity. Much effort has been made to improve CIK cells cytotoxicity and treatments of CIK cells combined with other antitumor therapies are applied. This review summarizes some strategies, including the combination of CIK with additional cytokines, dendritic cells, check point inhibitors, antibodies, chemotherapeutic agents, nanomedicines, and engineering CIK cells with a chimeric antigen receptor. Furthermore, we briefly sum up the clinical trials on CIK cells and compare the effect of clinical CIK therapy with other immunotherapies. Finally, further research is needed to clarify the pharmacological mechanism of CIK and provide evidence to formulate uniform culturing criteria for CIK expansion.

12.
Cell Mol Neurobiol ; 37(4): 707-715, 2017 May.
Artigo em Inglês | MEDLINE | ID: mdl-27443384

RESUMO

Previous studies have proven that paired immunoglobulin-like receptor B (PirB) plays a crucial suppressant role in neurite outgrowth and neuronal plasticity after central nervous system injury. However, the role of PirB in neuronal survival after cerebral ischemic injury and its mechanisms remains unclear. In the present study, the role of PirB is investigated in the survival and apoptosis of cerebral cortical neurons in cultured primary after oxygen and glucose deprivation (OGD)-induced injury. The results have shown that rebarbative PirB exacerbates early neuron apoptosis and survival. PirB gene silencing remarkably decreases early apoptosis and promotes neuronal survival after OGD. The expression of bcl-2 markedly increased and the expression of bax significantly decreased in PirB RNAi-treated neurons, as compared with the control- and control RNAi-treated ones. Further, phosphorylated TrkB and mTOR levels are significantly downregulated in the damaged neurons. However, the PirB silencing markedly upregulates phosphorylated TrkB and mTOR levels in the neurons after the OGD. Taken together, the overexpression of PirB inhibits the neuronal survival through increased neuron apoptosis. Importantly, the inhibition of the phosphorylation of TrkB and mTOR may be one of its mechanisms.


Assuntos
Apoptose , Sobrevivência Celular/efeitos dos fármacos , Córtex Cerebral/metabolismo , Neurônios/metabolismo , Receptores Imunológicos/metabolismo , Animais , Apoptose/efeitos dos fármacos , Hipóxia Celular/efeitos dos fármacos , Células Cultivadas , Regulação para Baixo/efeitos dos fármacos , Glucose/metabolismo , Glicoproteínas de Membrana/metabolismo , Fármacos Neuroprotetores/farmacologia , Oxigênio/metabolismo , Fosforilação , Proteínas Tirosina Quinases/metabolismo , Receptores Imunológicos/genética , Serina-Treonina Quinases TOR/metabolismo , Regulação para Cima/efeitos dos fármacos
13.
Environ Sci Pollut Res Int ; 23(21): 21451-21459, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27507143

RESUMO

The effect of no-tillage (NT) on rice yield and nitrogen (N) behavior often varies considerably from individual studies. A meta-analysis was performed to assess quantitatively the effect of NT on rice yield and N uptake by rice, N use efficiency (NUE, i.e., fertilizer N recovery efficiency), and nutrient runoff losses. We obtained data from 74 rice-field experiments reported during the last three decades (1983-2013). Results showed the NT system brought a reduction of 3.8 % in the rice yield compared with conventional tillage (CT). Soil pH of 6.5-7.5 was favorable for the improvement of rice yield with the NT system, while a significant negative NT effect on rice yield was observed in sandy soils (p < 0.05). N rate, ranging from 120 to 180 kg N ha-1, for at least 3 years was necessary for NT to enable rice yield comparable with that of CT. Furthermore, the observations indicated NT reduced N uptake and NUE of the rice by 5.4 and 16.9 %, while increased the N and P exports via runoff by 15.4 and 40.1 % compared with CT, respectively. Seedling cast transplantation, N rate within the range 120-180 kg N ha-1, and employing NT for longer than 3 years should be encouraged to compromise between productivity and environmental effects of NT implementation in rice fields.


Assuntos
Agricultura/métodos , Nitrogênio/metabolismo , Oryza/crescimento & desenvolvimento , Oryza/metabolismo , Poluentes Químicos da Água/análise , Fertilizantes/análise
14.
Environ Sci Pollut Res Int ; 23(9): 8598-609, 2016 May.
Artigo em Inglês | MEDLINE | ID: mdl-26797950

RESUMO

No tillage (NT) can be used as a management tool to alleviate the negative effects of agricultural practices on the environment by reducing the runoff volume and nutrient exports. The main objective of this research was to quantify the effect of NT on nitrogen (N) and phosphorus (P) exports across a rice-planted watershed using the soil and water assessment tool (SWAT) model. Results show that total N and P runoff exports from rice fields across the watershed ranged from 7.2 to 22.8 kg N/ha and 0.56 to 6.80 kg P/ha, respectively, over five rice-growing seasons under conventional tillage (CT) practice. The adoption of NT reduced the runoff volume, and the total N and total P exports by 25.9, 8.5, and 7.8 %, respectively, compared with the total exports under CT practice in the same study area. Rice yields were reduced by 0.7-1.9 % within the first 4 years after the adoption of NT, but began to rise in the fifth year. These results suggest that a long-term period of NT practice is necessary to reduce N and P exports without comprising the rice yield on rice-planted watersheds. In addition, the benefits of implementing NT practice alone were limited, and other practices, such as water and nutrient management, should be combined with NT practice.


Assuntos
Agricultura/métodos , Nitrogênio/análise , Oryza , Fósforo/análise , Poluentes Químicos da Água/análise , Monitoramento Ambiental , Modelos Químicos , Estações do Ano , Solo , Movimentos da Água
15.
Sci Rep ; 5: 16079, 2015 Nov 03.
Artigo em Inglês | MEDLINE | ID: mdl-26526140

RESUMO

High content of organic matter in the downstream of watersheds underscored the severity of non-point source (NPS) pollution. The major objectives of this study were to characterize and quantify dissolved organic matter (DOM) in watersheds affected by NPS pollution, and to apply self-organizing map (SOM) and parallel factor analysis (PARAFAC) to assess fluorescence properties as proxy indicators for NPS pollution and labor-intensive routine water quality indicators. Water from upstreams and downstreams was sampled to measure dissolved organic carbon (DOC) concentrations and excitation-emission matrix (EEM). Five fluorescence components were modeled with PARAFAC. The regression analysis between PARAFAC intensities (Fmax) and raw EEM measurements indicated that several raw fluorescence measurements at target excitation-emission wavelength region could provide similar DOM information to massive EEM measurements combined with PARAFAC. Regression analysis between DOC concentration and raw EEM measurements suggested that some regions in raw EEM could be used as surrogates for labor-intensive routine indicators. SOM can be used to visualize the occurrence of pollution. Relationship between DOC concentration and PARAFAC components analyzed with SOM suggested that PARAFAC component 2 might be the major part of bulk DOC and could be recognized as a proxy indicator to predict the DOC concentration.


Assuntos
Poluentes Químicos da Água/química , Qualidade da Água , Água/química , Monitoramento Ambiental , Análise Fatorial , Análise de Regressão , Espectrometria de Fluorescência , Água/análise , Poluentes Químicos da Água/análise
16.
Bioresour Technol ; 198: 746-54, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-26454040

RESUMO

Rice straw was used as a carbon source in a denitrifying bioreactor, for the removal of nutrients from agricultural drainage. Nutrient removal efficiency was evaluated by: (a) nutrient loading rates (low, medium, and high); (b) hydraulic retention time, and (c) comparison with another carbon source (woodchip). The results show that concentrations of nitrate nitrogen (NO3(-)-N), ammonia nitrogen (NH4(+)-N), total nitrogen (TN), and orthophosphate phosphorus (PO4(3-)-P) in the rice-straw bioreactor effluents were reduced by 53%, 25%, 40%, and 35%, respectively, compared with influents at the medium nutrient loading rate (NO3(-)-N: 10-15 mg N L(-1), NH4(+)-N: 10-15 mg N L(-1), PO4(3-)-P: 1.0-1.5 mg P L(-1)) and long hydraulic retention time (HRT, 24h), with a corresponding denitrification rate (DR) of 0.40 mg N L(-1)h(-1). Moreover, the rice-straw bioreactor showed significantly higher (p<0.05) nutrient removal efficiency than the woodchip bioreactor at the medium nutrient loading rate and 24h HRT.


Assuntos
Reatores Biológicos , Desnitrificação , Oryza/metabolismo , Carbono/metabolismo , Eutrofização , Nitratos/metabolismo , Nitrogênio/metabolismo , Fosfatos/metabolismo , Fósforo/metabolismo , Poluição da Água/prevenção & controle , Madeira/metabolismo
17.
Int J Mol Sci ; 16(9): 21846-57, 2015 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-26378518

RESUMO

DNA dioxygenases Ten-Eleven Translocation (TET) proteins can catalyze the conversion of 5-methylcytosine (5mC) of DNA to 5-hydroxymethylcytosine (5hmC), and thereby alter the epigenetic state of DNA. The TET family includes TET1, TET2 and TET3 members in mammals. Recently, accumulative research uncovered that TET1-3 occur abundantly in the central nervous system (CNS), and their biological functions have just begun to be investigated. In the present study, we demonstrated that mRNA and protein of TET2 were highly expressed in the cerebral cortex and hippocampus along the whole brain-development process. Further studies showed that TET2 was expressed in various types of cells, especially in most neurons. Subcellular distribution pattern implicated that TET2 is localized in both nucleus and cytoplasm of neurons. Down-regulation of TET2 in cultured cortical neurons with RNA interference implied that TET2 was required for cell survival. In all, our results indicate that neuronal TET2 is positively involved in the regulation of cell survival.


Assuntos
Sistema Nervoso Central/metabolismo , Proteínas de Ligação a DNA/metabolismo , Proteínas Proto-Oncogênicas/metabolismo , Animais , Sobrevivência Celular/genética , Córtex Cerebral/metabolismo , Proteínas de Ligação a DNA/genética , Expressão Gênica , Perfilação da Expressão Gênica , Camundongos , Neurônios/metabolismo , Transporte Proteico , Proteínas Proto-Oncogênicas/genética
18.
Sci Rep ; 5: 11445, 2015 Jun 18.
Artigo em Inglês | MEDLINE | ID: mdl-26086415

RESUMO

Excessive microglial activation often contributes to inflammation-mediated neurotoxicity in the ischemic penumbra during the acute stage of ischemic stroke. Toll-like receptor 4 (TLR4) has been reported to induce microglial activation via the NF-κB pathway. Isoflurane preconditioning (IP) can provide neuroprotection and inhibit microglial activation. In this study, we investigated the roles of the TLR4 signalling pathway in IP to exert neuroprotection following ischemic stroke in vivo and in vitro. The results showed that 2% IP alleviated neurological deficits, reduced the infarct volume, attenuated apoptosis and weakened microglial activation in the ischemic penumbra. Furthermore, IP down-regulated the expression of HSP 60, TLR4 and MyD88 and up-regulated inhibitor of IκB-α expression compared with I/R group in vivo. In vitro, 2% IP and a specific inhibitor of TLR4, CLI-095, down-regulated the expression of TLR4, MyD88, IL-1ß, TNF-α and Bax, and up-regulated IκB-α and Bcl-2 expression compared with OGD group. Moreover, IP and CLI-095 attenuated microglial activation-induced neuronal apoptosis, and overexpression of the TLR4 gene reversed the neuroprotective effects of IP. In conclusion, IP provided neuroprotection by regulating TLR4 expression directly, alleviating microglial activation and neuroinflammation. Thus, inhibiting the activation of microglial activation via TLR4 may be a new avenue for stroke treatment.


Assuntos
Regulação da Expressão Gênica/efeitos dos fármacos , Isoflurano/farmacologia , Microglia/efeitos dos fármacos , Microglia/metabolismo , Fármacos Neuroprotetores/farmacologia , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/metabolismo , Animais , Apoptose/efeitos dos fármacos , Biomarcadores , Infarto Encefálico/tratamento farmacológico , Infarto Encefálico/genética , Infarto Encefálico/metabolismo , Infarto Encefálico/patologia , Infarto Encefálico/fisiopatologia , Células Cultivadas , Chaperonina 60/metabolismo , Modelos Animais de Doenças , Expressão Gênica , Proteínas I-kappa B/metabolismo , Precondicionamento Isquêmico , Isoflurano/administração & dosagem , Masculino , Modelos Moleculares , Fator 88 de Diferenciação Mieloide/metabolismo , Inibidor de NF-kappaB alfa , Fármacos Neuroprotetores/administração & dosagem , Ratos , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/genética , Traumatismo por Reperfusão/metabolismo , Acidente Vascular Cerebral/tratamento farmacológico , Acidente Vascular Cerebral/genética , Acidente Vascular Cerebral/metabolismo , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/fisiopatologia , Receptor 4 Toll-Like/genética , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo
19.
Cell Mol Neurobiol ; 35(8): 1093-103, 2015 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-25976178

RESUMO

We have reported electroacupuncture (EA) pretreatment induced the tolerance against focal cerebral ischemia through activation of canonical Notch pathway. However, the underlying mechanisms have not been fully understood. Evidences suggest that up-regulation of hypoxia inducible factor-1α (HIF-1α) contributes to neuroprotection against ischemia which could interact with Notch signaling pathway in this process. Therefore, the current study is to test that up-regulation of HIF-1α associated with Notch pathway contributes to the neuroprotection of EA pretreatment. Sprague-Dawley rats were treated with EA at the acupoint "Baihui (GV 20)" 30 min per day for successive 5 days before MCAO. HIF-1α levels were measured before and after reperfusion. Then, HIF-1α antagonist 2ME2 and γ-secretase inhibitor MW167 were used. Neurologic deficit scores, infarction volumes, neuronal apoptosis, and Bcl2/Bax were evaluated. HIF-1α and Notch1 intracellular domain (NICD) were assessed. The results showed EA pretreatment enhanced the neuronal expression of HIF-1α, reduced infarct volume, improved neurological outcome, inhibited neuronal apoptosis, up-regulated expression of Bcl-2, and down-regulated expression of Bax after reperfusion in the penumbra, while the beneficial effects were attenuated by 2ME2. Furthermore, intraventricular injection with MW167 efficiently suppressed both up-regulation of NICD and HIF-1α after reperfusion. However, administration with 2ME2 could only decrease the expression of HIF-1α in the penumbra. In conclusion, EA pretreatment exerts neuroprotection against ischemic injury through Notch pathway-mediated up-regulation of HIF-1α.


Assuntos
Isquemia Encefálica/metabolismo , Isquemia Encefálica/prevenção & controle , Eletroacupuntura/métodos , Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese , Receptor Notch1/fisiologia , Regulação para Cima/fisiologia , Animais , Masculino , Ratos , Ratos Sprague-Dawley , Resultado do Tratamento
20.
PLoS One ; 9(3): e91019, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24614080

RESUMO

Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Lesões Encefálicas/patologia , Campos Eletromagnéticos , Éteres Metílicos/farmacologia , Neurônios/patologia , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Animais , Comportamento Animal/efeitos dos fármacos , Lesões Encefálicas/complicações , Lesões Encefálicas/tratamento farmacológico , Caspase 3/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Córtex Cerebral/patologia , Cognição/efeitos dos fármacos , L-Lactato Desidrogenase/metabolismo , Masculino , Malondialdeído/metabolismo , Éteres Metílicos/uso terapêutico , Degeneração Neural/complicações , Degeneração Neural/tratamento farmacológico , Degeneração Neural/patologia , Neurônios/efeitos dos fármacos , Neurônios/enzimologia , Neurônios/ultraestrutura , Ratos Sprague-Dawley , Sevoflurano , Superóxido Dismutase/metabolismo , Proteína X Associada a bcl-2/metabolismo
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