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1.
Zhongguo Zhong Yao Za Zhi ; 42(7): 1390-1394, 2017 Apr.
Artigo em Zh | MEDLINE | ID: mdl-29052404

RESUMO

To discuss the effects of total glucosides from white paeony on preventing and treating radioactive liver damage, and explore its possible mechanisms. Thirty-six patients with primary hepatic carcinoma from 105th Hospital of Chinese PLA were treated with 3-dimensional conformal radiotherapy and randomly divided into simple irradiation group, total glucosides from white paeony group, and control group. The levels of AST, ALT, HA, LN, PCⅢ, CIV and TGF-ß1 in serum of various groups were determined by using ELISA method. As compared with the simple irradiation group and control group, total glucosides from white paeony could obviously decrease the levels of AST, ALT, HA, LN, PCⅢ, CIV and TGF-ß1(P<0.05, P<0.01). The results showed that the total glucosides from white paeony could effectively prevent and treat radioactive liver damage, and its mechanism might be associated with decreasing the levels of TGF-ß1, and inhibiting the synthesis of collagen synthesis.


Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Glucosídeos/farmacologia , Fígado/efeitos da radiação , Paeonia/química , Lesões por Radiação/tratamento farmacológico , Humanos , Fígado/efeitos dos fármacos , Fator de Crescimento Transformador beta1/sangue , Resultado do Tratamento
2.
J Neuroinflammation ; 12: 246, 2015 Dec 30.
Artigo em Inglês | MEDLINE | ID: mdl-26715049

RESUMO

BACKGROUND: Acid-sensing ion channels (ASICs) are cation channels which were activated by extracellular acidosis and involved in various physiological and pathological processes in the nervous system. Inflammasome is a key component of the innate immune response in host against harmful and irritable stimuli. As the first discovered molecular platform, NLRP1 (nucleotide-binding oligomerization domain (NOD)-like receptor protein 1) inflammasome is expressed in neurons and implicated in many nervous system diseases such as brain injury, nociception and epilepsy. However, little is known about the effect of ASICs on NLRP1 inflammasome activation under acidosis. METHODS: The expression of inflammasome complex protein (NLRP1, ASC (apoptosis-associated speck-like protein containing a caspase-activating recruitment domain) and caspase-1), inflammatory cytokines (IL-1ß and IL-18), and apoptosis-related protein (Bax, Bcl-2, and activated caspase-3) was detected by Western blot. Large-conductance Ca(2+) and voltage-activated K(+) (BK) channel currents were recorded by whole-cell patch-clamp technology. Measurement of [K(+)] i was performed by fluorescent ion imaging system. Co-expression of ASICs and BK channels was determined by dual immunofluorescence. Cell viability was assessed by MTT and LDH kit. RESULTS: ASICs and BK channels were co-expressed in primary cultured cortical neurons. Extracellular acidosis increased the expression of NLRP1, ASC, caspase-1, IL-1ß, and IL-18. Further mechanistic studies revealed that acidosis-induced ASIC1a activation results in the increase of BK channel currents, with the subsequent K(+) efflux and a low concentration of intracellular K(+), which activated NLRP1 inflammasome. Furthermore, these effects of acidosis could be blocked by specific ASIC1a inhibitor PcTX1 and BK channel inhibitor IbTX. The data also demonstrated neutralization of NLRP1-protected cortical neurons against injury induced by extracellular acidosis. CONCLUSIONS: Our data showed that NLRP1 inflammasome could be activated by extracellular acidosis though ASIC-BK channel K(+) signal pathway and was involved in extracellular acidosis-induced cortical neuronal injury.


Assuntos
Canais Iônicos Sensíveis a Ácido/metabolismo , Acidose/metabolismo , Córtex Cerebral/metabolismo , Líquido Extracelular/metabolismo , Proteínas do Tecido Nervoso/metabolismo , Neurônios/metabolismo , Animais , Animais Recém-Nascidos , Sobrevivência Celular/fisiologia , Células Cultivadas , Inflamassomos/metabolismo , Ratos , Ratos Sprague-Dawley
3.
Zhong Yao Cai ; 35(4): 603-7, 2012 Apr.
Artigo em Zh | MEDLINE | ID: mdl-23019909

RESUMO

OBJECTIVE: To study the mechanism of protective effect of Fagopyrum cymosum on lung injury induced by Klebsiella pneumonia in rats. METHODS: The model of rats with Klebsiella pneumonia was established. The male SD rats were randomly divided into control group, model group, Fagopyrum cymosum (6, 3, 1.5 g/kg) three groups, levofloxacin (25 mg/kg) group. The pathological change of lung was observed. The content of IL-1beta, IL-6, IL-8, TNF-alpha, ICAM-1, INF-gamma in serum were measured by radioimmunoassay and Elisa. TNF-alpha, ICAM-1, NF-kappaB p65 protein expressions were measured by immunohistochemistry. MIP-2mRNA expression was detected by in situ hybridization. RESULTS: The rats of model group had obvious lung injury, but those of Fagopyrum cymosum and levofloxacin groups had less injury. The contents of IL-1beta, IL-6, IL-,8, TNF-alpha, ICAM-1 and INF-gamma in serum and the expressions of TNF-a, ICAM-1, NF-kappaB p65 and MIP--2mRNA of model group were significantly higher than those of the control group (P < 0.05 or P < 0.01), while the indexes of Fagopyrum cymosum and levofloxacin groups were significantly lower than those of model group (P < 0.05 or P < 0.01). CONCLUSION: The lung injury induced by Klebsiella pneumonia is related to TNF-alpha, ICAM-1, NF-kappaB p65 and MIP-2mRNA. To decrease the excessive expression of TNF-alpha, ICAM-1, NF-kappaB p65 and MIP-2mRNA might be the main mechanism of protective effect of Fagopyrum cymosum on lung injury.


Assuntos
Citocinas/metabolismo , Medicamentos de Ervas Chinesas/administração & dosagem , Fagopyrum , Infecções por Klebsiella/tratamento farmacológico , Pulmão/metabolismo , Pneumonia Bacteriana/tratamento farmacológico , Animais , Quimiocina CXCL2/genética , Quimiocina CXCL2/metabolismo , Citocinas/sangue , Modelos Animais de Doenças , Medicamentos de Ervas Chinesas/farmacologia , Fagopyrum/química , Imuno-Histoquímica , Infecções por Klebsiella/sangue , Infecções por Klebsiella/metabolismo , Infecções por Klebsiella/microbiologia , Klebsiella pneumoniae/efeitos dos fármacos , Levofloxacino , Pulmão/efeitos dos fármacos , Pulmão/microbiologia , Masculino , Ofloxacino/administração & dosagem , Ofloxacino/farmacologia , Pneumonia Bacteriana/sangue , Pneumonia Bacteriana/metabolismo , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley
4.
World J Gastroenterol ; 14(45): 6936-42, 2008 Dec 07.
Artigo em Inglês | MEDLINE | ID: mdl-19058328

RESUMO

AIM: To investigate the effects and possible mechanisms of Wy14643 on hepatic ischemia-reperfusion (I/R) injury in rats. METHODS: Thirty male Sprague-Dawley rats weighing 220-280 g were randomly divided into five experimental groups: sham group (G1, n=6): a sham operation was performed (except for liver I/R); I/R-untreated group (G2, n=6): rats underwent liver ischemia for 90 min followed by reperfusion for 4 h; and I/R+Wy14643 groups (G3, G4, G5; n=6): after the same surgical procedure as in group 2, animals were pretreated with Wy14643 at the dose of 1, 5 and 10 mg/kg 1 h before ischemia, respectively. Hepatic ischemia-reperfusion (I/R) was induced by clamping blood supply to the left lateral and median lobes of the liver for 90 min, and atraumatic clamp was removed for 4 h reperfusion. Blood samples and liver tissues were obtained at the end of reperfusion to assess serum and hepatic tissue homogenate aminotransferase (ALT), aspartate aminotransferase (AST), myeloperoxidase (MPO), serum interleukin-1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha), as well as activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA) in the hepatic tissue homogenate. RESULTS: Hepatic I/R induced a significant increase in the serum levels of ALT, AST, TNF-alpha, IL-1beta and MPO, as well as the levels of ALT, AST and MDA in the liver tissue homogenate, which were reduced by pretreatment with Wy14643 at the dose of 1, 5 and 10 mg/kg, respectively. The activity of SOD in the liver tissue homogenate was decreased after hepatic I/R, which was enhanced by Wy14643 pretreatment. In addition, serum and liver tissue homogenate ALT and AST in the Wy14643 10 mg/kg group were lower than in the Wy14643 1 mg/kg and 5 mg/kg groups, respectively. CONCLUSION: Wy14643 pretreatment exerts significant protection against hepatic I/R injury in rats. The protective effects are possibly associated with enhancement of anti-oxidant and inhibition inflammation response.


Assuntos
Hepatite/prevenção & controle , PPAR alfa/agonistas , Pirimidinas/uso terapêutico , Traumatismo por Reperfusão/prevenção & controle , Alanina Transaminase/metabolismo , Animais , Aspartato Aminotransferases/metabolismo , Modelos Animais de Doenças , Hepatite/metabolismo , Hepatite/patologia , Interleucina-1beta/sangue , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Masculino , Malondialdeído/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Peroxidase/metabolismo , Pirimidinas/farmacologia , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia , Superóxido Dismutase/metabolismo , Fator de Necrose Tumoral alfa/sangue
5.
Am J Chin Med ; 36(2): 385-97, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18457368

RESUMO

This study was aimed at investigating the protective effect and mechanism of vitexin preconditioning (VPC) on cultured neonatal rat cardiomyocytes after anoxia and reoxygenation (A/R). An A/R model was established by using cultured neonatal rat cardiomyocytes. Cellular injury was evaluated by measuring cell viability, the releases of creatine kinase (CK), and lactate dehydrogenase (LDH). The apoptosis rate of cardiomyocytes after Anoxia/reoxygenation and the activities of extracellular signal-regulated protein kinases (ERKs) were measured. The intracellular calcium indicated by the fluorescence in cardiomyocytes was measured by the laser confocal microscope. Vitexin preconditioning (10, 30 and 100 microM) significantly enhanced the cell viability, markedly inhibited A/R-induced increases of LDH and CK release, obviously decreased the number of apoptotic cardiomyocytes and markedly decreased the fluorescence intensity value of [Ca(2+)](i) in cardiomyocytes. Exposure to anoxia or vitexin preconditioning significantly increased the phospho-ERK level, and the increase was markedly inhibited by PD98059, an inhibitor of the upstream kinase of ERK. These results suggest that vitexin preconditioning has a protective effect on cardiomyocytes A/R injury through the improvement of cell viability, decrease of LDH and CK release, such that the protective mechanism may relate to its ability to inhibit the cardiomyocytes apoptosis, reduce the cardiomyocytes calcium overload and increase the abundance of phosphor-ERK1/2 of the cardiomyocytes after anoxia and reoxygenation.


Assuntos
Apigenina/farmacologia , Hipóxia Celular , Precondicionamento Isquêmico Miocárdico , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Miócitos Cardíacos/citologia , Animais , Animais Recém-Nascidos , Apoptose/efeitos dos fármacos , Cálcio/metabolismo , Sobrevivência Celular , Células Cultivadas , Creatina Quinase/metabolismo , L-Lactato Desidrogenase/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Miócitos Cardíacos/metabolismo , Ratos , Ratos Sprague-Dawley
6.
Zhongguo Zhong Yao Za Zhi ; 33(12): 1463-5, 2008 Jun.
Artigo em Zh | MEDLINE | ID: mdl-18837357

RESUMO

OBJECTIVE: To investigate the protective effects of injection of Danhong against acute myocardial ischemia in dogs. METHOD: The myocardial ischemia model were established by ligation of coronary artery in dogs. The degree of myocardial ischemia and the myocardial infarction size were observed before and after giving injection of Danhong. The serum creatine phosphokinase (CK) and lactate dehydrogenase (LDH) activities were also determined. RESULT: Injection of Danhong (1, 2, 4 g x kg(-1)) could significantly decreased the damage degree of myocardial ischemia, redused myocardial infarction size and also reduced the serum LDH and CK activities. CONCLUSION: Injection of Danhong had protective action on myocardial ischemia.


Assuntos
Medicamentos de Ervas Chinesas/administração & dosagem , Medicamentos de Ervas Chinesas/farmacologia , Isquemia Miocárdica/prevenção & controle , Animais , Creatina Quinase/sangue , Cães , Injeções , L-Lactato Desidrogenase/sangue , Infarto do Miocárdio/sangue , Infarto do Miocárdio/complicações , Infarto do Miocárdio/patologia , Isquemia Miocárdica/sangue , Isquemia Miocárdica/complicações , Isquemia Miocárdica/tratamento farmacológico
7.
Neurosci Res ; 55(2): 142-5, 2006 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-16616791

RESUMO

The modulatory effect of Total Flavone of Abelmoschus manihot L. Medic (TFA) on NMDA-activated current (I(NMDA)) was investigated in cultured rat hippocampal neurons using the whole-cell patch-clamp technique. TFA rapidly and reversibly inhibited the I(NMDA) in a concentration-dependent manner. Furthermore, TFA non-competitively inhibited the I(NMDA) by enhancement of the NMDA receptor desensitization. In addition, intracellular application of TFA did not alter the TFA inhibition of I(NMDA). These results suggest that the inhibition of the NMDA receptor response by TFA could be one of the mechanisms for TFA-mediated neuroprotective actions.


Assuntos
Abelmoschus/química , Flavonoides/farmacologia , Hipocampo/citologia , Inibição Neural/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Receptores de N-Metil-D-Aspartato/fisiologia , Animais , Animais Recém-Nascidos , Células Cultivadas , Relação Dose-Resposta a Droga , Interações Medicamentosas , Estimulação Elétrica/métodos , Agonistas de Aminoácidos Excitatórios/farmacologia , Flavonas , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/fisiologia , Potenciais da Membrana/efeitos da radiação , N-Metilaspartato/farmacologia , Neurônios/fisiologia , Técnicas de Patch-Clamp/métodos , Ratos , Ratos Wistar
8.
Am J Chin Med ; 34(3): 483-92, 2006.
Artigo em Inglês | MEDLINE | ID: mdl-16710897

RESUMO

This study was to investigate the effect of total flavones of rhododendra (TFR) on ischemic myocardial injury in rabbits. Rabbit ischemic myocardial injury was induced by occluding the anterior descent of the left artery (LAD). The ECG was recorded; the plasma creatine kinase (CK), nitric oxide (NO) and endothelin-1 (ET-1) levels were measured using spectrophotometry, Griess method and radioimmunoassay, respectively. The myocardial ischemic size and infarction size were determined by dual staining with Evan's blue and Nitroblue tetrazolium reductionest (N-BT). A typical ECG S-T segment elevation and an increase of plasma CK activity were observed 6 and 24 hours after the induction of ischemia. These changes were inhibited in rabbits treated with either TFR (30, 60 mg/kg) or ginkgo biloba extract (EGB) for 7 days, indicating a protective effect of TFR on ischemic myocardial injury. The myocardial ischemic size and infarction size were 40.7 +/- 3.6% and 36.8 +/- 3.6% respectively in the control group, while TFR (60 mg/kg) pretreatment for 7 days significantly reduced both myocardial ischemic size (32.40 +/- 5.38%, p < 0.05) and infarction size (28.7 +/- 5.8%, p < 0.05). In addition, the occlusion of LAD resulted in an increase of ET-1 and a decrease of NO levels in the plasma, effects that were inhibited by TFR treatment, suggesting a possible mechanism for the protective effect of TFR against myocardial ischemic injury.


Assuntos
Flavonas/farmacologia , Isquemia Miocárdica/prevenção & controle , Extratos Vegetais/farmacologia , Rhododendron/química , Animais , Creatina Quinase/sangue , Eletrocardiografia , Endotelinas/sangue , Isquemia Miocárdica/fisiopatologia , Óxido Nítrico/sangue , Coelhos
9.
Chin J Integr Med ; 11(1): 57-9, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15975311

RESUMO

OBJECTIVE: To study the effects of total flavone of Abelmoschl Manihot L. Medic (TFA) on the function of platelets and to explore its mechanism. METHODS: Rat models of artery-veins bypassing thrombus formation were used. The platelets of rabbits were collected. Platelet aggregation was induced by collagen and intracellular calcium ion concentration ([Ca(2+)]i) was assayed by Fura-2 method. RESULTS: TFA (25, 50, 100 mg/kg) significantly and dose-dependently reduced the weight of thrombus. TFA (0.025, 0.05, 0.1 mg/ml) possessed dose-dependant inhibitory effects on rabbits' platelet aggregation induced by collagen. TFA significantly reduced the resting and CaCl(2)-induced increase of free intracellular calcium concentration ([Ca(2+)]i) in rabbit platelet in vitro. CONCLUSION: TFA has an antiplatelet effect via the inhibition on the influx of Ca(2+).


Assuntos
Plaquetas/efeitos dos fármacos , Bloqueadores dos Canais de Cálcio/farmacologia , Trombose das Artérias Carótidas/sangue , Medicamentos de Ervas Chinesas/farmacologia , Flavonas/farmacologia , Glicosídeos/farmacologia , Inibidores da Agregação Plaquetária/farmacologia , Animais , Cálcio/sangue , Bloqueadores dos Canais de Cálcio/administração & dosagem , Cloreto de Cálcio/farmacologia , Trombose das Artérias Carótidas/etiologia , Colágeno/farmacologia , Relação Dose-Resposta a Droga , Medicamentos de Ervas Chinesas/administração & dosagem , Flavonas/administração & dosagem , Glicosídeos/administração & dosagem , Membranas Intracelulares/metabolismo , Concentração Osmolar , Agregação Plaquetária/efeitos dos fármacos , Inibidores da Agregação Plaquetária/administração & dosagem , Testes de Função Plaquetária , Coelhos/sangue , Ratos , Ratos Wistar
10.
Yao Xue Xue Bao ; 39(3): 176-9, 2004 Mar.
Artigo em Zh | MEDLINE | ID: mdl-15171650

RESUMO

AIM: To investigate the effects of total lactones of ginkgo on aging by using D-galactose induced aging mice and natural aging mice. METHODS: By using D-galactose induced aging mice, to detect the LF content in heart and liver, the Hyp content in liver, the MAO, GSH-Px activities and the NO content in cerebrum. The apoptosis of cerebral cell was determined by terminal deoxy-nucleotidyl transforase-mediated dUTP-digoxigenin nick end-labeling (Tunel) in natural aging mice. RESULTS: TLG was shown to increase the GSH-Px activities, reduce the NO content and decrease the MAO activity in cerebrum. Meanwhile, TLG was found to reduce the LF content in liver and heart and raise the Hyp content in liver. TLG was shown to inhibit apoptosis of cerebral cell and decrease the number of apoptotic cells in the brain. CONCLUSION: TLG possesses effect on antiaging via attenuating lipid peroxidation and NO and apoptosis of cerebral cells.


Assuntos
Envelhecimento/metabolismo , Apoptose/efeitos dos fármacos , Ginkgo biloba , Lactonas/farmacologia , Animais , Feminino , Galactose , Ginkgo biloba/química , Glutationa Peroxidase/metabolismo , Hidroxiprolina/metabolismo , Lactonas/isolamento & purificação , Lipofuscina/metabolismo , Fígado/metabolismo , Masculino , Camundongos , Monoaminoxidase/metabolismo , Miocárdio/metabolismo , Óxido Nítrico/metabolismo , Plantas Medicinais/química , Telencéfalo/enzimologia , Telencéfalo/metabolismo
11.
Life Sci ; 107(1-2): 21-6, 2014 Jun 27.
Artigo em Inglês | MEDLINE | ID: mdl-24792518

RESUMO

AIMS: This study was aimed to determine whether microRNA1 (miR1) plays a role in the activation of myosin light chain kinase (MLCK) mediated by oxLDL in human umbilical vein endothelial cells (HUVECs). MAIN METHODS: HUVECs were treated with oxLDL along with a control miR or miR1 mimic. MiR1 expression was assayed by miRNA plate assay kit and mirVana™ miRNA isolation kit. The MLCK protein, transcript, and kinase activity were measured by Western blot, real-time-polymerase chain reaction and γ-(32)P-ATP phosphate incorporation, respectively. In addition, phosphorylation of MLC, ERK and p38 was analyzed by Western blot. KEY FINDINGS: The results showed that upon treatment with oxLDL, miR1 expression was decreased, whereas MLCK expression was increased, in a time- and dose-dependent manner. Consistent with this, miR1 mimic prevented MLCK expression and activation and attenuated the phosphorylation of MLC and ERK/p38 in oxLDL-treated HUVECs. Furthermore, we showed that miR1 was able to bind a site located at the 3'un-translational region of MLCK mRNA and inhibited its expression. SIGNIFICANCE: Taken together, this study demonstrated that the effect of miR1 on hyperlipidemia is mediated through down-regulation of MLCK and the ERK/p38 MAPK pathway.


Assuntos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Hiperlipidemias/metabolismo , Lipoproteínas LDL/farmacologia , MicroRNAs/fisiologia , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Quinase de Cadeia Leve de Miosina/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Apoptose/efeitos dos fármacos , Western Blotting , Proliferação de Células/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Hiperlipidemias/tratamento farmacológico , Hiperlipidemias/patologia , Luciferases/metabolismo , Proteínas de Membrana/antagonistas & inibidores , Proteínas de Membrana/metabolismo , Quinase de Cadeia Leve de Miosina/genética , Fosforilação/efeitos dos fármacos , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais/efeitos dos fármacos
12.
Int J Cardiol ; 176(3): 764-70, 2014 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-25131924

RESUMO

BACKGROUND: High-fat diet has been reported to be associated with cardiovascular diseases which is implicated in atherosclerosis. However, the underlying mechanisms remain unknown. MicroRNAs (miRNAs) are non-coding small RNAs that control gene expression at the post-transcriptional level. Dysregulated miRNAs have been shown to be involved in atherosclerosis. METHODS AND RESULTS: This study examined whether microRNA-29b (miR-29b) regulates high-fat diet induced endothelial permeability and apoptosis by targeting MT1, a known melatonin membrane receptor. In apoE knock-out mice, a high-fat diet increased miR-29b expression and induced apoptosis as determined by up-regulation of caspase-3 activity. However, a standard diet did not alter apoptosis. miR-29b antagomir decreased endothelial permeability and apoptosis in high-fat diet-stimulated mice. In contrast, a miR-29b mimic enhanced endothelial permeability and apoptosis. The induction of miR-29b correlated with a reduction in Bcl-2 and MT1 in high-fat diet-stimulated mice. miR-29b have an effect on the marker of inflammation (NF-κB) and cell adhesion molecule (ICAM-1). We further showed that miR-29b targeted and inhibited MT1 expression through a target site located in the 3'un-translational region of MT1 mRNA. This study demonstrates a role of miR-29b in atherosclerosis and identifies MT1 as a direct target of miR-29b. CONCLUSIONS: The effect of miR-29b on endothelial permeability and apoptosis is mediated through the down-regulation of MT1. Thus, miR-29b may be a new therapeutic target for atherosclerosis.


Assuntos
Apolipoproteínas E/deficiência , Permeabilidade Capilar/fisiologia , Dieta Hiperlipídica/efeitos adversos , Endotélio Vascular/metabolismo , MicroRNAs/biossíntese , Receptor MT1 de Melatonina/biossíntese , Animais , Apoptose/fisiologia , Regulação para Baixo/fisiologia , Regulação da Expressão Gênica , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Masculino , Camundongos , Camundongos Knockout , Distribuição Aleatória
13.
Am J Chin Med ; 41(6): 1251-66, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24228599

RESUMO

This study was conducted to demonstrate myocardial protective effects and possible underlying mechanisms of vitexin on myocardial ischemia/reperfusion (I/R) injury in rats. Occluding the anterior descending artery for 30 min and restoring blood perfusion for 60 min in rat established a model of myocardial I/R. The elevation of the ST segment of Electrocardiograph (ECG) was observed. The infarct size of the rat heart was assessed by triphenyltetrazolium chloride staining (TTC). LDH, CK, SOD activities and MDA content were determined. An immunohistochemical analysis was applied to measure the expression of myocardial NF-κBp65 and TNF-α. ERK/phospho-ERKand c-Jun/phospho-c-Jun protein expression was examined via Western Blot. Vitexin significantly reduced the elevation of the ST segment of ECG and myocardial infarct size. LDH and CK activities and MDA content were attenuated in serum, while SOD activity was markedly enhanced. Vitexin significantly attenuated I/R-induced increases of myocardial NF-κB and TNF-α. Moreover, Western Blot analysis presented that vitexin markedly enhanced the expression of phospho-ERK and weakened the expression of phospho-c-Jun compared to I/R group. The significant protective effect against myocardial ischemical/reperfusion injury in rat, which is exhibited by vitexin, may be related to its antioxidative and anti-inflammatory effects by regulating inflammatory cytokines and the MAPK pathway.


Assuntos
Apigenina/administração & dosagem , Apigenina/farmacologia , Cardiotônicos , Citocinas/metabolismo , Mediadores da Inflamação/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases/genética , Isquemia Miocárdica/diagnóstico , Isquemia Miocárdica/tratamento farmacológico , Traumatismo por Reperfusão Miocárdica/diagnóstico , Traumatismo por Reperfusão Miocárdica/tratamento farmacológico , Fitoterapia , Animais , Modelos Animais de Doenças , Regulação para Baixo , Eletrocardiografia , Expressão Gênica/efeitos dos fármacos , Infusões Intravenosas , Masculino , Isquemia Miocárdica/genética , Isquemia Miocárdica/patologia , Traumatismo por Reperfusão Miocárdica/genética , Traumatismo por Reperfusão Miocárdica/patologia , Proteínas Proto-Oncogênicas c-jun/genética , Proteínas Proto-Oncogênicas c-jun/metabolismo , Ratos , Ratos Sprague-Dawley , Fator de Transcrição RelA/genética , Fator de Transcrição RelA/metabolismo , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Regulação para Cima
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