Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 5 de 5
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Exp Ther Med ; 18(6): 4820-4828, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31772647

RESUMO

Dexmedetomidine (DEX) is widely used in perioperative settings for analgesia and sedation; however, little is known about its effects on the hypoxia-induced progression of tumor cells. In the present study, the effects of DEX on hypoxia-induced growth and metastasis of lung cancer cells and colorectal cancer cells was examined. A549 cells and HCT116 cells were treated with normoxia, hypoxia, co-treatment of hypoxia and DEX, and atipamezole (an α2 adrenoceptor antagonist) for 4 h. The proliferation rate of cells was determined by MTT assays. Cell metastatic potential was evaluated by Transwell assays. Survivin and hypoxia inducible factor (HIF)-1α were detected by western blotting. Matrix metalloproteinase (MMP)-2 and MMP-9 were measured using reverse transcription-quantitative PCR. It was demonstrated that hypoxia treatment promoted the proliferation and may promote the metastasis of the two cancer cell lines. DEX substantially contributed to the survival and aggressiveness of the two cancer cell lines following hypoxia. Furthermore, DEX upregulated the expression of survivin, MMP-2, MMP-9 and HIF-1α in the two cancer cell lines in response to hypoxia. Finally, the effects of DEX on the hypoxia-induced growth and metastatic potential of cancer cells were reversed by atipamezole. Collectively, DEX enhances the hypoxia-induced progression of lung cancer cells and colorectal cancer cells by regulating HIF-1α signaling, which may be associated with the α2 adrenoceptor pathway.

2.
Eur J Pharmacol ; 812: 18-27, 2017 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-28668506

RESUMO

Acute kidney injury caused by ischemia-reperfusion injury (IRI) is a major risk factor for chronic kidney disease, which is characterized by renal interstitial fibrosis. However, the molecular mechanisms underlying renal fibrosis induced by IRI are not fully understood. Our results showed that interleukin (IL)-33 was induced markedly after IRI insult, and the kidneys of mice following IRI plus IL-33 treatment presented more severe renal fibrosis compared with mice treated with IRI alone. Therefore, we investigated whether inhibition of IL-33 protects against IRI-induced renal fibrosis. Mice were administrated with soluble ST2 (sST2), a decoy receptor that neutralizes IL-33 activity, or vehicle by intraperitoneal injection for 14 days after IRI challenge. We revealed that mice treated with sST2 exhibited less severe renal dysfunction and fibrosis in response to IRI compared with vehicle-treated mice. Inhibition of IL-33 suppressed bone marrow-derived fibroblast accumulation and myofibroblast formation in the kidneys after IRI stress, which was associated with less expression of extracellular matrix proteins. Furthermore, inhibition of IL-33 also showed a significant reduction of F4/80+ macrophages and CD3+ T cells in the kidneys of mice after IRI treatment. Finally, Treatment with IL-33 inhibitor reduced proinflammatory cytokine and chemokine levels in the kidneys of mice following IRI insult. Taken together, our findings indicate that IL-33 signaling plays a critical role in the pathogenesis of IRI-induced renal fibrosis through regulating myeloid fibroblast accumulation, inflammation cell infiltration, and the expression of proinflammatory cytokines and chemokines.


Assuntos
Interleucina-33/metabolismo , Rim/patologia , Traumatismo por Reperfusão/patologia , Transdução de Sinais , Animais , Fibrose , Rim/metabolismo , Macrófagos/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Traumatismo por Reperfusão/imunologia , Traumatismo por Reperfusão/metabolismo , Linfócitos T/imunologia , Linfócitos T/metabolismo
3.
J Clin Anesth ; 35: 304-312, 2016 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27871548

RESUMO

STUDY OBJECTIVE: Platelets play a pivotal role in metastasis of tumor cells. The aim of this study is to explore the effects of sevoflurane and isoflurane on platelets activation of patients undergoing lung cancer surgery, and the effects of sevoflurane and isoflurane on platelets-induced invasion of lung cancer cells. DESIGN: Prospective and randomized study, and in vitro experiment. SETTING: University-affiliated teaching hospital and laboratory. PATIENTS: Forty-six patients scheduled for lung cancer radical surgery. INTERVENTIONS: Patients were randomized to two groups of 23 patients each and were received sevoflurane (group SEV) or isoflurane (group ISO) during surgery, respectively. In vitro, lung cancer cells were treated with platelets in the presence or absence anesthetics. MEASUREMENTS: Platelets activation were determined by detecting glycoproteinIIb/IIIa (GPIIb/IIIa), CD62P, and platelets aggregation rate (PAR) pre-, intra-, and postoperatively. Invasion ability of lung cancer cells were evaluated by Transwell assay. RESULTS: The levels of GPIIb/IIIa, CD62P, and PAR were reduced markedly in group SEV during perioperative period compared with group ISO. In vitro, activated platelets contributed profoundly to the invasive ability of lung cancer cells. Sevoflurane, but not isoflurane, inhibited platelets-induced invasion of lung cancer cells. Furthermore, sevoflurane suppressed the platelets activity in vitro. CONCLUSION: Sevoflurane attenuates platelets activation of patients undergoing lung cancer surgery. In vitro, sevoflurane suppresses platelets-induced invasion of lung cancer cells via decreasing platelets activity.


Assuntos
Anestésicos Inalatórios/farmacologia , Plaquetas/patologia , Isoflurano/farmacologia , Neoplasias Pulmonares/patologia , Éteres Metílicos/farmacologia , Ativação Plaquetária/efeitos dos fármacos , Células A549 , Idoso , Anestesia Geral , Anestésicos Inalatórios/administração & dosagem , Humanos , Isoflurano/administração & dosagem , Neoplasias Pulmonares/sangue , Neoplasias Pulmonares/imunologia , Neoplasias Pulmonares/cirurgia , Masculino , Éteres Metílicos/administração & dosagem , Pessoa de Meia-Idade , Invasividade Neoplásica/imunologia , Selectina-P/análise , Agregação Plaquetária/efeitos dos fármacos , Complexo Glicoproteico GPIIb-IIIa de Plaquetas/análise , Pneumonectomia/métodos , Estudos Prospectivos , Sevoflurano , Toracoscopia
4.
Neuroreport ; 24(3): 131-6, 2013 Feb 13.
Artigo em Inglês | MEDLINE | ID: mdl-23370493

RESUMO

TRESK gene recombinant adenovirus (10 IU/ml), which has been constructed successfully in our previous study, was implemented through an intrathecal injection. The fact that the method can effectively upregulate the expression of TRESK mRNA in the dorsal root ganglia of spared nerve injury in rats was verified. We also investigated the role of TRESK gene recombinant adenovirus in attenuating tactile allodynia and thermal hyperalgesia in spared nerve injury rats. Spared nerve injury to the sciatic nerve induced persistent tactile allodynia, but had no effect on thermal hyperalgesia. Intrathecal injection of TRESK gene recombinant adenovirus (25 µl) into the region of lumbar enlargement in advance reduced tactile allodynia. Moreover, intrathecal injection of TRESK gene recombinant adenovirus (25 µl) significantly alleviated the activation of astrocytes in spinal cord induced by spared nerve injury. The current study shows that an intrathecal injection of the TRESK gene recombinant adenovirus attenuated the activity of astrocytes in spinal cord, which contributed to relieving neuropathic pain in spared nerve injury rats. According to the result reported in our previous study, attenuating the expression of TRESK in dorsal root ganglia was involved in the development of neuropathic pain. On the basis of these results, we theorized that the therapeutic utility of upregulation of TRESK in dorsal root ganglia was effective in relieving neuropathic pain syndromes induced by peripheral nerve injury.


Assuntos
Adenoviridae/genética , Canais de Potássio/uso terapêutico , Ciática/tratamento farmacológico , Animais , Astrócitos/metabolismo , Astrócitos/patologia , Modelos Animais de Doenças , Gânglios Espinais/metabolismo , Vetores Genéticos , Proteína Glial Fibrilar Ácida/metabolismo , Hiperalgesia/tratamento farmacológico , Injeções Espinhais , Masculino , Medição da Dor , Canais de Potássio/biossíntese , Canais de Potássio/genética , RNA Mensageiro/metabolismo , Ratos , Ratos Sprague-Dawley , Ciática/patologia , Medula Espinal/metabolismo
5.
Mol Med Rep ; 5(4): 1049-52, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22307830

RESUMO

The present study was conducted to determine whether the activation of TRESK in the dorsal root ganglion (DRG) by the TRESK gene recombinant adenovirus vector inhibits the capsaicin-evoked substance P (SP) release using a radioimmunoassay. TRESK is an outwardly rectifying K+ current channel that contributes to the resting potential and is the most important background potassium channel in DRG. Previous studies have shown that neuropathic pain (NP) is closely related to the regulation of certain potassium channels in DRG neurons, while DRG-released SP is important in the peripheral mechanism of NP. In the present study, the TRESK gene adenovirus vector significantly enhanced the TRESK mRNA and protein of the cultured rat DRG neurons. Radioimmunoassay analysis revealed that the capsaicin­mediated SP release was significantly inhibited by the TRESK gene recombinant adenovirus vector in rat DRG neurons. These findings suggest that TRESK plays a role in adjusting the release of SP in DRG, which is related to NP.


Assuntos
Adenoviridae/genética , Antipruriginosos/farmacologia , Capsaicina/farmacologia , Gânglios Espinais/efeitos dos fármacos , Vetores Genéticos , Canais de Potássio/metabolismo , Substância P/metabolismo , Animais , Células Cultivadas , Gânglios Espinais/citologia , Neurônios/citologia , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Canais de Potássio/genética , Ratos , Ratos Sprague-Dawley
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA