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1.
Int. microbiol ; 22(3): 317-323, sept. 2019. graf
Artigo em Inglês | IBECS | ID: ibc-184838

RESUMO

In recent years, the beneficial impact of targeted gut microbiota manipulation in various neurological disorders has become more evident. Therefore, probiotics have been considered as a promising approach to modulate brain gene expression and neuronal pathways even in some neurodegenerative diseases. The purpose of this study was to determine the effect of probiotic biotherapy with combination of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 on the expression levels of proteins critical to neuronal apoptosis in hippocampus of lipopolysaccharide (LPS)-exposed rats. Four groups of animals (Control, LPS, Probiotic + LPS, and Probiotic) were treated with maltodextrin (placebo) or probiotic (109 CFU/ml/rat) for 2 weeks by gavage. On the 15th day, a single intraperitoneal dose of saline or LPS (1 mg/kg) was injected and 4 h later, protein assessment was performed by western blotting in hippocampal tissues. LPS significantly increased the Bax, Bax/Bcl-2 ratio, and cleaved caspase-3 expression along with decreased the Bcl-2 and procaspase-3 protein levels. However, probiotic pretreatment (L. helveticus R0052 + B. longum R0175) significantly downregulated the Bax and Bax/Bcl-2 ratio accompanied with upregulated Bcl-2 expression. Prophylactic treatment with these bacteria also attenuated LPS-induced caspase-3 activation by remarkably increasing the expression of procaspase-3 while reducing the level of cleaved caspase-3 in target tissues. Our data indicate that probiotic formulation (L. helveticus R0052 + B. longum R0175) alleviated hippocampal apoptosis induced by LPS in rats via the gut-brain axis and suggest that this probiotic could play a beneficial role in some neurodegenerative conditions


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Assuntos
Animais , Ratos , Apoptose , Bifidobacterium longum/crescimento & desenvolvimento , Hipocampo/patologia , Lactobacillus helveticus/crescimento & desenvolvimento , Probióticos/administração & dosagem , Western Blotting , Caspase 3/análise , Hipocampo/efeitos dos fármacos , Lipopolissacarídeos/toxicidade , Placebos/administração & dosagem , Proteínas Proto-Oncogênicas c-bcl-2/análise , Proteína X Associada a bcl-2/análise
2.
J. physiol. biochem ; 72(4): 721-732, dic. 2016. graf, ilus
Artigo em Inglês | IBECS | ID: ibc-168379

RESUMO

MicroRNAs (miRNAs) are endogenous, non-coding, small RNAs, which play a critical role in regulating varieties of the biological and pathologic processes. miR-181a has been reported to participate in tumorigenic progression. However, the roles of miR-181a in cervical cancer (CC) are still unknown. The aim of this research was to explore the effects and molecular mechanism of miR-181a in CC cells. In this paper, the levels of miR-181a in CC cell lines were determined by real-time PCR. We found that the levels of miR-181a were evidently enhanced in CC cell lines compared with normal cervical epithelium cells. Then, the miR-181a inhibitor was transiently transfected into HeLa and CaSKi cells using Lipofectamine 2000 reagent. Subsequently, the Cell Counting Kit-8 (CCK-8) and BrdU-ELISA results showed that down-regulation of miR-181a inhibited the cell viability and proliferation. Our data also demonstrated that miR-181a inhibitor arrested cell cycle progression of HeLa and CaSKi cells by up-regulation of p21 and p27 expressions. In addition, inhibition of miR-181a promoted apoptosis of HeLa and CaSKi cells due to increasing Bax expression and decreasing Bcl-2 expression. Ultimately, the effect of miR-181a inhibitor on the PTEN/Akt/FOXO1 signaling pathway was investigated by Western blot. From our results, down-regulation of miR-181a increased the expression of PTEN and decreased phosphorylation of Akt and FOXO1. Altogether, miR-181a might be an oncogene in CC cells. The potential mechanism was that inhibition of miR-181a might suppress proliferation and invasion and promote apoptosis of HeLa and CaSKi cells by modulating the PTEN/Akt/FOXO1 signaling pathway (AU)


No disponible


Assuntos
Humanos , Feminino , Colo do Útero/metabolismo , MicroRNAs/genética , Proteína Forkhead Box O1/genética , Regulação Neoplásica da Expressão Gênica , PTEN Fosfo-Hidrolase/genética , Proteínas Proto-Oncogênicas c-akt/genética , Fenômenos Fisiológicos Celulares , Linhagem Celular Tumoral , Células Epiteliais , Oligorribonucleotídeos , Transdução de Sinais , Inibidor de Quinase Dependente de Ciclina p21 , Proteína X Associada a bcl-2
3.
J. physiol. biochem ; 72(3): 381-392, sept. 2016. tab, graf, ilus
Artigo em Inglês | IBECS | ID: ibc-168282

RESUMO

The prostate gland is a part of the male reproductive tract which produces both angiotensin II (Ang II) and relaxin 2 (RLN2). The present study analyzes the effect of both these peptide hormones at concentration 10−8M on viability, proliferation, adhesion, migration, and invasion of normal prostate epithelial cells (PNT1A). Improved survival in two- and three-dimensional cell cultures was noted as well as visual changes in colony size and structure in Geltrex™. Stimulatory influence on cell viability of each peptide applied single was lower than in combination. Enhanced survival of PNT1A cells appears to be associated with increased BCL2/BAX messenger RNA (mRNA) expression ratio. Modulation of cell spreading and cell-extracellular matrix adhesion dynamics were also altered as an influence of tested hormone application. However, long-term Ang II and RLN2 effects may lead to an increase of normal prostate cell migration and invasion abilities. Moreover, gelatin zymography revealed that both gelatinases A and B were augmented by Ang II treatment, whereas RLN2 significantly stimulated only MMP-9 secretion. These results support the hypothesis that deregulation of locally secreted peptide hormones such as Ang II and RLN2 may take part in the development of certain cancers, including prostate cancer. Moreover, the observed ability of relaxin 2 to act as a regulator of mRNA expression levels not only LGR7 but also classic angiotensin receptors suggested that renin-angiotensin system and relaxin family peptide system are functionally linked (AU)


No disponible


Assuntos
Humanos , Masculino , Apoptose , Angiotensina II/metabolismo , Regulação da Expressão Gênica , Membrana Mucosa/metabolismo , Próstata/metabolismo , Relaxina/metabolismo , Membrana Basal/fisiologia , Fenômenos Fisiológicos Celulares , Metaloproteinase 2 da Matriz , Metaloproteinase 9 da Matriz , Receptor Tipo 1 de Angiotensina , Receptor Tipo 2 de Angiotensina , Proteínas Proto-Oncogênicas c-bcl-2 , Receptores Acoplados a Proteínas-G , Proteína X Associada a bcl-2 , RNA Mensageiro/metabolismo , Receptores de Peptídeos
5.
Clin. transl. oncol. (Print) ; 15(7): 582-586, jul. 2013. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-127472

RESUMO

BACKGROUND: Currently, first-line chemotherapy in advanced colorectal cancer is not tailored on predictive biomarkers. Bax proapoptotic protein may correlate to chemosensitivity and differential response to irinotecan or oxaliplatin-based combinations. METHODS: Bax expression was assessed by immunohistochemistry in 49 advanced colorectal cancer patients enrolled at our institution from 2002 to 2004 within a multicenter, phase II, randomized trial of first-line UFT/leucovorin/irinotecan (TEGAFIRI) versus UFT/leucovorin/oxaliplatin (TEGAFOX). RESULTS: Bax-positive and negative samples were 49 and 51 %. Response was significantly lower in Bax positive (25 %) as compared to Bax negative (56 %) (Odds ratio = 0.26; p = 0.03). No significant difference was noted in TEGAFOX subgroup; in TEGAFIRI arm, responses were lower in Bax positive (18 %) than Bax negative (67 %) (Odds ratio = 0.11; p = 0.03). No difference in terms of progression-free and overall survival was observed according to Bax. CONCLUSION: Bax-negative colorectal cancer may identify a specific phenotype of patients with significantly higher chance to respond to doublet irinotecan-based chemotherapy (AU)


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Antineoplásicos/uso terapêutico , Camptotecina/análogos & derivados , Neoplasias Colorretais/tratamento farmacológico , Proteína X Associada a bcl-2/metabolismo , Antineoplásicos/administração & dosagem , Camptotecina/uso terapêutico , Neoplasias Colorretais/patologia , Intervalo Livre de Doença , Imuno-Histoquímica
6.
Med. clín (Ed. impr.) ; 140(11): 508-513, jun. 2013. ilus
Artigo em Espanhol | IBECS | ID: ibc-112478

RESUMO

La infección por el virus de la hepatitis B genera frecuentemente una inflamación crónica del hígado, que evoluciona a cirrosis y hepatocarcinoma en un elevado porcentaje de pacientes. La activación persistente del sistema inmunitario origina un daño hepático continuado que estimula de forma desorganizada fenómenos de reparación y remodelado tisular. La proteína viral X (HBx) es imprescindible para la replicación del virus y, por tanto, para el mantenimiento crónico de la infección. El principal potencial oncogénico de HBx reside, por una parte, en su capacidad para integrarse al ADN celular, y por otra, en la transactivación de diversas vías de señalización implicadas en crecimiento celular, apoptosis y reparación del ADN. Además, HBx interacciona con el proteasoma y es capaz de modificar la homeostasis del calcio celular. Esta revisión analiza el papel de HBx en la progresión de la hepatitis crónica B a través de sus efectos en procesos angiogénicos, fibrogénicos y oncogénicos (AU)


The infection by hepatitis B virus often promotes chronic liver inflammation which progresses to cirrhosis and hepatocellular carcinoma in a high percentage of patients. The persistent activation of the immune system causes an incessant liver damage, which fosters a disorganized stimulation of tissue repair and remodelling phenomena. In turn, the viral protein X (HBx) is essential for virus replication and therefore for the maintenance of chronic infection. However, the important oncogenic potential of HBx seems to reside, on one hand, in its ability to integrate into cellular DNA and, additionally, in the transactivation of different cellular signaling pathways involved in cell growth regulation, apoptosis and DNA repair. HBx also interacts with proteasome subunits and notably affects mitochondrial electric potential, thus altering cellular calcium homeostasis. Finally, this review discusses the pathogenic role of HBx in the progression of chronic hepatitis B through its effects on angiogenic, fibrogenic and oncogenic processes (AU)


Assuntos
Humanos , Vírus da Hepatite B/patogenicidade , Hepatite B Crônica/fisiopatologia , Proteína X Associada a bcl-2/análise , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia
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