Base de dados : LILACS
Pesquisa : D08.811.913.696.620.500 [Categoria DeCS]
Referências encontradas : 15 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 2 ir para página        

  1 / 15 LILACS  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1136283
Autor: Guo, Hong-Li; Chen, Gang; Song, Ze-Long; Sun, Jia; Gao, Xi-Hai; Han, Yu-Xia.
Título: COL6A3 promotes cellular malignancy of osteosarcoma by activating the PI3K/AKT pathway
Fonte: Rev. Assoc. Med. Bras. (1992);66(6):740-745, June 2020. graf.
Idioma: en.
Resumo: SUMMARY OBJECTIVE In this study, we aimed to investigate the role of COL6A3 on cell motility and the PI3K/AKT signaling pathway in osteosarcoma. METHODS The relative expression of COL6A3 was achieved from a GEO dataset in osteosarcoma tissue. siRNA technology was applied to decrease the COL6A3 expression in cells, and cell counting kit-8 (CCK-8) assay and colony formation analysis were used to examine the cell proliferation potential. Knockdown COL6A3 made the proliferation and colony formation abilities worse than the COL6A3 without interference. Likewise, in contrast to the si-con group, cell invasion and migration were inhibited in the si-COL6A3 group. Moreover, the western blot results suggested that the PI3K/AKT signaling pathway was manipulated by measuring the protein expression of the PI3K/AKT pathway-related markers, due to the COL6A3 inhibition. CONCLUSION COL6A3 plays a crucial role in modulating various aspects of the progression of osteosarcoma, which would provide a potentially effective treatment for osteosarcoma.

RESUMO OBJETIVO Neste estudo, investigamos a função do COL6A3 na mobilidade celular e na via PI3K/AKT em osteossarcomas. METODOLOGIA A expressão relativa do COL6A3 foi obtida a partir de dados GEO em tecidos de osteossarcoma. O RNA de interferência (siRNA) foi utilizado para reduzir a expressão do COL6A3 nas células, e o teste de contagem de células kit-8 (CCK-8) e a análise de formação de colônias foram realizados para examinar o potencial de proliferação celular. Além disso, o Transwell comprovou os efeitos do si-COL6A3 na invasão celular e migração em células de osteossarcoma. Para medir os níveis de expressão das proteínas e mRNAs, utilizamos transcriptase reversa quantitativa (qRT-PCR) e western blot. RESULTADOS O COL6A3 foi regulado nos tecidos e células do osteossarcoma quando comparado com o controle normal. A redução de COL6A3 reduziu a proliferação e a capacidades de formação de colônias em relação ao COL6A3 sem interferência. Do Mesmo modo, ao contrário do observado no grupo si-con, a invasão e migração celular foram inibidas no grupo si-COL6A3. Além disso, o resultado do western blot sugere que a via PI3K/AKT foi manipulada, medindo a expressão proteica dos marcadores relacionados à PI3K/AKT, devido à inibição do COL6A3. CONCLUSÃO O COL6A3 desempenha um papel crucial na modulação de vários aspectos da progressão do osteossarcoma, o que pode representar um possível tratamento eficaz para a doença.
Descritores: Neoplasias Ósseas
Osteossarcoma
-Fosfatidilinositol 3-Quinases
Colágeno Tipo VI
Linhagem Celular Tumoral
Proliferação de Células
Proteínas Proto-Oncogênicas c-akt
Limites: Humanos
Responsável: BR1.1 - BIREME


  2 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1136287
Autor: Li, Ming; Wang, Jiu-Fei; Liu, Bo; Wang, Xiao-Min.
Título: Homeobox B2 is a potential prognostic biomarker of glioblastoma
Fonte: Rev. Assoc. Med. Bras. (1992);66(6):794-799, June 2020. graf.
Idioma: en.
Resumo: SUMMARY OBJECTIVES HOXB2 is a new prognostic indicator for lung cancer. But it is unclear whether HOXB2 holds an effect in glioblastoma (GBM) progression. The purpose of this article was to probe the influences of HOXB2 on GBM pathogenesis. METHODS HOXB2 expression level and prognostic power in GBM patients were analyzed. Then the mRNA and protein expression levels of HOXB2 in GBM cell lines were tested by qRT-PCR and western blotting. Cell proliferation, invasion, and migration were determined by CCK8 and transwell assay, severally. The protein levels of PI3K/AKT-pathway associated proteins were analyzed by western blotting. RESULTS The results indicated that HOXB2 was distinctly overexpressed in GBM patients and high expression of HOXB2 was related to a poor prognosis. Moreover, the expression of HOXB2 was higher in all GBM cell lines U251, U-87MG, GOS-3 than that in HEB cells (normal control). Meanwhile, decreased expression of p-PI3K and p-AKT were identified after HOXB2 knockdown. CONCLUSIONS These data demonstrated that HOXB2 had a vital role in GBM progression and could serve as a promising target for GBM treatment.

RESUMO OBJETIVOS A HOXB2 é um novo indicador prognóstico para o câncer de pulmão. Mas não está claro se a HOXB2 tem algum efeito na progressão do glioblastoma (GBM). O objetivo deste artigo foi sondar as influências da HOXB2 na patogênese do GBM. MÉTODOS Foram analisados o nível de expressão e o poder prognóstico da HOXB2 em pacientes com GBM. Em seguida, os níveis de expressão proteica e mRNA da HOXB2 em linhagens de células de GBM foram testados por qRT-PCR e western blotting. A proliferação, a invasão e migração celular foram determinadas por CCK8 e ensaios transwell, várias vezes. Os níveis proteicos das proteínas associadas à via PI3K/AKT foram analisados pelo método western blotting. RESULTADOS Os resultados indicaram que havia uma clara superrexpressão da HOXB2 em pacientes com GBM e que a alta expressão da HOXB2 estava relacionada a um prognóstico negativo. Além disso, a expressão da HOXB2 foi mais elevada em todas as linhagens de células do GBM U251, U-87MG, GOS-3 do que nas células HEB (controle normal). Entretanto, a diminuição da expressão de P-PI3K e p-AKT foi identificada após a redução da expressão da HOXB2. CONCLUSÕES Esses dados demonstram que a HOXB2 desempenha um papel vital na progressão do GBM, podendo ser um alvo promissor para o tratamento do GBM.
Descritores: Neoplasias Encefálicas/diagnóstico
Genes Homeobox/fisiologia
Glioblastoma/diagnóstico
-Prognóstico
Biomarcadores
Regulação Neoplásica da Expressão Gênica
Fosfatidilinositol 3-Quinases
Linhagem Celular Tumoral
Proliferação de Células
Limites: Humanos
Responsável: BR1.1 - BIREME


  3 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Id: biblio-1051305
Autor: Wang, Heyuan; Wu, Bing; Wang, Haotian.
Título: Alpha-hederin induces the apoptosis of oral cancer SCC-25 cells by regulating PI3K/Akt/mTOR signaling pathway
Fonte: Electron. j. biotechnol;38:27-31, Mar. 2019. graf, ilus.
Idioma: en.
Projeto: Jilin Provincial Industrial Innovation Special Fund Project; . Jilin Province Chinese Medicine Science and Technology.
Resumo: BACKGROUND: Oral cancer is one of the common malignant tumors of the head and neck. However, current treatments have numerous side effects, and drugs from natural sources may have better therapeutic potential. This research investigated the induction of apoptosis by α-hederin (α-HN), a constituent of Pulsatilla chinensis (Bunge) Regel, in the oral cancer cell line SCC-25 and its underlying mechanism. RESULTS: SCC-25 cells were treated with 50, 100, and 200 µmol/L α-HN. Cell proliferation; extent of apoptosis; activities of caspases-3, 8, and 9; and the expression of Bcl-2, Bax, phosphorylated (p)-phosphoinositide 3-kinase (PI3K), p-Akt, and p-mammalian target of rapamycin (mTOR) proteins were determined using the 3-(4,5)-2-thiazole-(2,5)-diphenyl tetrazolium bromide, flow cytometry, caspase activity detection kits, and western blot assays, respectively. The results showed that the proliferation of SCC-25 cells in the α-HN-treated groups decreased significantly, and the inhibitory effect was time and concentration dependent. Compared with cells in the control group, the extent of apoptosis increased significantly, caspase-3 and -9 activities were significantly enhanced, and the Bcl-2 level was lowered and the Bax level was elevated significantly in SCC-25 cells treated with α-HN for 48 h (P b 0.05). The expression of p-PI3K, p-Akt, and p-mTOR was also significantly lower in SCC-25 cells treated with α-HN than that in the control group (P b 0.05). CONCLUSION: These results indicate that α-HN can inhibit proliferation and induce apoptosis of SCC-25 cells and may exert these effects by inhibiting the PI3K/Akt/mTOR signaling pathway.
Descritores: Ácido Oleanólico/análogos & derivados
Saponinas/farmacologia
Neoplasias Bucais/metabolismo
Apoptose/efeitos dos fármacos
-Ácido Oleanólico/metabolismo
Ácido Oleanólico/farmacologia
Saponinas/metabolismo
Transdução de Sinais/efeitos dos fármacos
Sobrevivência Celular
Western Blotting
Fosfatidilinositol 3-Quinases/metabolismo
Caspases
Pulsatilla
Proliferação de Células/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Citometria de Fluxo
Neoplasias de Cabeça e Pescoço/metabolismo
Responsável: CL1.1 - Biblioteca Central


  4 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1011396
Autor: Ai, Xuejun; Xiang, Lei; Huang, Zhi; Zhou, Shi; Zhang, Shuai; Zhang, Tao; Jiang, Tianpeng.
Título: Overexpression of PIK3R1 promotes hepatocellular carcinoma progression
Fonte: Biol. Res;51:52, 2018. tab, graf.
Idioma: en.
Projeto: National Natural Science Foundation of China; . Scientific Cooperation in Guizhou Province.
Resumo: BACKGROUND: Phosphoinositide-3-kinase, regulatory subunit 1 (PIK3R1) could regulate cancer cell proliferation important for cancer cell proliferation; however, its role in Hepatocellular carcinoma (HCC) remains largely unknown. Here, we investigated the role of PIK3R1 in HCC and examined the underlying molecular mechanisms. METHODS: The expression of PIK3R1 was evaluated by immunohistochemistry and qRT-PCR in a series of HCC tissues. The mRNA and protein expression of PIK3R1 was used by qRT-PCR and western blot assays in a series of human HCC cell lines, and then we choose MHCC97H and HCCLM3 cells as a model to investigate the effect of PIK3R1 on HCC progression. The effects of PIK3R1 knowdown on cell proliferation, migration, apoptosis of HCC were assessed by the MTT assay, clonogenic assays, wound healing assay and flow cytometry in vitro. Western blot assay was performed to assess the expression changes of PI3K/AKT/mTOR signaling pathway. RESULTS: Our results found that PIK3R1 was highly expressed in HCC tissues compared with adjacent normal tissues. Knockdown of PIK3R1 inhibited the proliferation, migration and promoted apoptosis of HCC cell lines. In addition, we proved that knockdown of PIK3R1 downregulated p-PI3K, p-AKT, and p-mTOR expressions in MHCC97H and HCCLM3 cells. CONCLUSIONS: In conclusion, PIK3R1 providing potential novel targets for the treatment of HCC.
Descritores: Regulação Neoplásica da Expressão Gênica/genética
Carcinoma Hepatocelular/genética
Fosfatidilinositol 3-Quinases/genética
Neoplasias Hepáticas/genética
-Imuno-Histoquímica
Western Blotting
Apoptose
Carcinoma Hepatocelular/patologia
Progressão da Doença
Linhagem Celular Tumoral
Proliferação de Células
Classe Ia de Fosfatidilinositol 3-Quinase
Reação em Cadeia da Polimerase em Tempo Real
Neoplasias Hepáticas/patologia
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  5 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1011410
Autor: Liu, Xiaoli; Jiang, Qingfeng; Liu, Huaimin; Luo, Suxia.
Título: Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells
Fonte: Biol. Res;52:7, 2019. graf.
Idioma: en.
Resumo: BACKGROUND: Currently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms. RESULTS: The experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator. CONCLUSIONS: Accordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.
Descritores: Apoptose/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/patologia
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Apigenina/farmacologia
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Serina-Treonina Quinases TOR/efeitos dos fármacos
Neoplasias Pulmonares/patologia
Antineoplásicos/farmacologia
-Transdução de Sinais/efeitos dos fármacos
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Células A549
Neoplasias Pulmonares/metabolismo
Camundongos Nus
Mitocôndrias/efeitos dos fármacos
Limites: Humanos
Animais
Camundongos
Responsável: CL1.1 - Biblioteca Central


  6 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Chile
Texto completo
Id: biblio-1011428
Autor: Feng, Yubin; Hua, Xiaoxiao; Niu, Ruowen; Du, Yan; Shi, Congjian; Zhou, Renpeng; Chen, Fei-Hu.
Título: ROS play an important role in ATPR inducing differentiation and inhibiting proliferation of leukemia cells by regulating the PTEN/PI3K/AKT signaling pathway
Fonte: Biol. Res;52:26, 2019. graf.
Idioma: en.
Projeto: National Major Scientific and Technological Special Project.
Resumo: BACKGROUND: Acute myeloid leukemia (AML) is an aggressive and mostly incurable hematological malignancy with frequent relapses after an initial response to standard chemotherapy. Therefore, novel therapies are urgently required to improve AML clinical outcomes. 4-Amino-2-trifluoromethyl-phenyl retinate (ATPR), a novel all-trans retinoic acid (ATRA) derivative designed and synthesized by our team, has been proven to show biological anti-tumor characteristics in our previous studies. However, its potential effect on leukemia remains unknown. The present research aims to investigate the underlying mechanism of treating leukemia with ATPR in vitro. METHODS: In this study, the AML cell lines NB4 and THP-1 were treated with ATPR. Cell proliferation was analyzed by the CCK-8 assay. Flow cytometry was used to measure the cell cycle distribution and cell differentiation. The expression levels of cell cycle and differentiation-related proteins were detected by western blotting and immunofluorescence staining. The NBT reduction assay was used to detect cell differentiation. RESULTS: ATPR inhibited cell proliferation, induced cell differentiation and arrested the cell cycle at the G0/G1 phase. Moreover, ATPR treatment induced a time-dependent release of reactive oxygen species (ROS). Additionally, the PTEN/PI3K/Akt pathway was downregulated 24 h after ATPR treatment, which might account for the anti-AML effects of ATPR that result from the ROS-mediated regulation of the PTEN/PI3K/AKT signaling pathway. CONCLUSIONS: Our observations could help to develop new drugs targeting the ROS/PTEN/PI3K/Akt pathway for the treatment of AML.
Descritores: Retinoides/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Antineoplásicos/farmacologia
-Fluorimunoensaio
Leucemia Mieloide Aguda
Transdução de Sinais
Regulação para Baixo
Diferenciação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/metabolismo
Linhagem Celular Tumoral
Proliferação de Células/efeitos dos fármacos
PTEN Fosfo-Hidrolase/efeitos dos fármacos
PTEN Fosfo-Hidrolase/metabolismo
Proteínas Proto-Oncogênicas c-akt/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


  7 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
Texto completo
Id: biblio-912717
Autor: Ferreira, Darkle Modesto; Neves, Tercia J; Lima, Luiz Guilherme C A; Alves, Fabio Abreu; Begnami, Maria Dirley.
Título: Prognostic implications of the phosphatidylinositol 3-kinase/Akt signaling pathway in oral squamous cell carcinoma: overexpression of p-mTOR indicates an adverse prognosis
Fonte: Appl. cancer res;37:1-8, 2017. tab, ilus.
Idioma: en.
Resumo: Background: The development of oral cavity cancer is related to the accumulation of genetic alterations. The activation of AKT is associated with the proliferation and progression of many malignancies. It is thought that MAP kinases, together with the PI3K/AKT/mTOR signaling pathway, promote uncoordinated proliferation via inhibition of PTEN, thus increasing cell survival and mediating cancer progression. However, there are few studies regarding the expression of these proteins in oral squamous cell carcinoma (SCC). Methods: The expression of PI3K, p-mTOR, p-AKT, p-MAPK, and PTEN in 125 oral SCCs, including gingival, palate hard, and alveolar ridge tumors, was examined by immunohistochemistry and correlated with clinicopathological data and survival rates. Results: We observed PI3K, p-mTOR, p-MAPK, p-AKT, and PTEN positive staining in the cytoplasm of most SCC (92.4%, 88.2%, 88.3%, 94.2%, and 25%, respectively). Positive nuclear staining was observed for p-mTOR, PTEN, p-AKT, and p-MAPK (42.9%, 72%, 64.2%, and 58.2%, respectively). Only p-mTOR protein expression was observed on the cell membrane and was present in 44.5% of cases. A statistically significant correlation was found between p-MAPK expression and SCC clinicopathological stages III and IV (p = 0.0042). Lower rates of disease-free survival were found in patients with SCC III / IV (p = 0.001). Patients with positive nuclear staining of p-mTOR displayed a significant increase in disease-free survival rates. Discussion: The identification of prognostic and predictive markers is clinically important because oral cancer is a group of heterogeneous diseases with various biological and clinical characteristics. Conclusion: Our findings suggest that the PI3K/AKT pathway is activated in gingival, hard palate, and alveolar ridge SCCs. We have demonstrated that p-mTOR expression can function as a biomarker for survival in oral SCCs and could be a promising therapeutic target in oral SCC treatment (AU)
Descritores: Prognóstico
Neoplasias Bucais/diagnóstico
Imuno-Histoquímica
Carcinoma de Células Escamosas/terapia
Biomarcadores Tumorais
Fosfatidilinositol 3-Quinases
PTEN Fosfo-Hidrolase
Aurora Quinase C
Limites: Humanos
Masculino
Feminino
Pessoa de Meia-Idade
Idoso
Idoso de 80 Anos ou mais
Responsável: BR30.1 - Biblioteca


  8 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1054685
Autor: Hou, Bao; Cai, Weiwei; Chen, Ting; Zhang, Zhixuan; Gong, Haifeng; Yang, Wei; Qiu, Liying.
Título: Vaccarin hastens wound healing by promoting angiogenesis via activation of MAPK/ERK and PI3K/AKT signaling pathways in vivo
Fonte: Acta cir. bras;34(12):e201901202, 2019. graf.
Idioma: en.
Projeto: Wuxi Science and Technology Development Fund 2018; . Jiangnan University Youth Fund 2018.
Resumo: Abstract Purpose To explore the potential role and unclear molecular mechanisms of vaccarin in wound healing. Methods Rats' skin excision model to study the effects of vaccarin on wound healing in vivo . Hematoxylin and eosin staining was performed to evaluate Histopathologic characteristics. Immunohistochemistry was employed to assess the effects of vaccarin in accelerating angiogenesis. Western blot was used to evaluate relative protein expressed levels. Results Vaccarin could significantly promote wound healing and endothelial cells and fibroblasts proliferation in the wound site. Immunohistochemistry and Western blot studies showed that the nodal proteins and receptor (bFGFR) related to angiogenesis signaling pathway were activated, and the microvascular density in the wound site was markedly higher than that in the control group. Conclusions The present study was the first to demonstrate that vaccarin is able to induce angiogenesis and accelerate wound healing in vivo by increasing expressions of p-Akt, p-Erk and p-bFGFR. This process is mediated by MAPK/ERK and PI3K/AKT signaling pathways.
Descritores: Cicatrização/efeitos dos fármacos
Extratos Vegetais/farmacologia
Fosfatidilinositol 3-Quinases/efeitos dos fármacos
Quinases de Proteína Quinase Ativadas por Mitógeno/efeitos dos fármacos
Caryophyllaceae/química
Indutores da Angiogênese/farmacologia
-Fatores de Tempo
Imuno-Histoquímica
Extratos Vegetais/química
Transdução de Sinais
Western Blotting
Reprodutibilidade dos Testes
Ratos Sprague-Dawley
Fosfatidilinositol 3-Quinases/análise
Quinases de Proteína Quinase Ativadas por Mitógeno/análise
Células Endoteliais/efeitos dos fármacos
Proliferação de Células/efeitos dos fármacos
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/análise
Receptor Tipo 1 de Fator de Crescimento de Fibroblastos/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


  9 / 15 LILACS  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-983682
Autor: Li, Qingwen; Cui, Shanshan; Jing, Guoqing; Ding, Huang; Xia, Zhongyuan; He, Xianghu.
Título: The role of PI3K/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion
Fonte: Acta cir. bras;34(1):e20190010000005, 2019. graf.
Idioma: en.
Resumo: Abstract Purpose: To investigate the role of PI3k/Akt signal pathway in the protective effects of propofol on intestinal and lung injury induced by intestinal ischemia/reperfusion(I/R). Methods: Male Sprague-Dawley rats were subjected to 45 min of ischemia by occluding the superior mesenteric artery and to 2h of reperfusion to establish the model of I/R. Twenty four rats were randomly divided into four groups: Sham, intestinal I/R (II/R), propofol (P), wortmannin (W). In groups P, W, propofol was injected intravenously and continuously at the onset of reperfusion via infusion pump. PI3K inhibitor (wortmannin) was administered intravenously in group W 25 min before ischemia. Intestinal tissues and lung tissues were obtained for determination of histologic injury, wet/dry weight ratio, malondialdehyde (MDA) levels, superoxide dismutase (SOD) and myeloperoxidase (MPO) activities. Meanwhile, the expressions of caspase-3 and phosphorylated Akt (p-Akt) in intestines and lungs were detected by western blot. Results: Propofol treatment alleviated intestinal and lung morphological changes which were observed in II/R group,Moreover, wet/dry weight ratio, the MDA level, MPO activity and expression of caspase-3 were significantly decreased whereas the SOD activity and p-Akt expression were significantly increased. Notably, the protections were significantly reversed by pretreatment of wortmannin. Conclusion: PI3K/Akt pathway activation play a critical role in the protective effects of propofol on intestinal and lung injury induced by ischemia/reperfusion.
Descritores: Traumatismo por Reperfusão/tratamento farmacológico
Propofol/farmacologia
Anestésicos Intravenosos/farmacologia
Fosfatidilinositol 3-Quinases/fisiologia
Proteínas Proto-Oncogênicas c-akt/fisiologia
Lesão Pulmonar/prevenção & controle
Isquemia Mesentérica/tratamento farmacológico
-Traumatismo por Reperfusão/metabolismo
Transdução de Sinais/fisiologia
Ratos Sprague-Dawley
Modelos Animais de Doenças
Isquemia Mesentérica/metabolismo
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


  10 / 15 LILACS  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
Texto completo
Id: biblio-1038128
Autor: Xiao, Jian-Min; Wang, Ji-Jia; Sun, Li-Li.
Título: Effect of miR-134 against myocardial hypoxia/reoxygenation injury by directly targeting NOS3 and regulating PI3K/Akt pathway
Fonte: Acta cir. bras;34(8):e201900802, 2019. tab, graf.
Idioma: en.
Resumo: Abstract Purpose To reveal the function of miR-134 in myocardial ischemia. Methods Real-time PCR and western blotting were performed to measure the expression of miR-134, nitric oxide synthase 3 (NOS3) and apoptotic-associated proteins. Lactic dehydrogenase (LDH) assay, cell counting kit-8 (CCK-8), Hoechst 33342/PI double staining and flow cytometry assay were implemented in H9c2 cells, respectively. MiR-134 mimic/inhibitor was used to regulate miR-134 expression. Bioinformatic analysis and luciferase reporter assay were utilized to identify the interrelation between miR-134 and NOS3. Rescue experiments exhibited the role of NOS3. The involvement of PI3K/AKT was assessed by western blot analysis. Results MiR-134 was high regulated in the myocardial ischemia model, and miR-134 mimic/inhibitor transfection accelerated/impaired the speed of cell apoptosis and attenuated/exerted the cell proliferative prosperity induced by H/R regulating active status of PI3K/AKT signaling. LDH activity was also changed due to the different treatments. Moreover, miR-134 could target NOS3 directly and simultaneously attenuated the expression of NOS3. Co-transfection miR-134 inhibitor and pcDNA3.1-NOS3 highlighted the inhibitory effects of miR-134 on myocardial H/R injury. Conclusion This present work puts insights into the crucial effects of the miR-134/NOS3 axis in myocardial H/R injury, delivering a potential therapeutic technology in future.
Descritores: Traumatismo por Reperfusão Miocárdica/metabolismo
MicroRNAs/metabolismo
Óxido Nítrico Sintase Tipo III/metabolismo
Hipóxia/metabolismo
-Traumatismo por Reperfusão Miocárdica/genética
Traumatismo por Reperfusão Miocárdica/patologia
Traumatismo por Reperfusão Miocárdica/tratamento farmacológico
Transdução de Sinais/efeitos dos fármacos
Apoptose/efeitos dos fármacos
Apoptose/fisiologia
Fosfatidilinositol 3-Quinases/metabolismo
MicroRNAs/genética
MicroRNAs/uso terapêutico
Proliferação de Células/efeitos dos fármacos
Óxido Nítrico Sintase Tipo III/genética
Óxido Nítrico Sintase Tipo III/uso terapêutico
Proteínas Proto-Oncogênicas c-akt/metabolismo
Limites: Animais
Ratos
Responsável: BR1.1 - BIREME



página 1 de 2 ir para página        
   


Refinar a pesquisa
  Base de dados : Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde