ABSTRACT
Objective: To explore therapeutic effect of fructose-1, 6-diphosphate (FDP) combined antiviral treatment on pediatric patients with viral myocarditis (VMC). Methods: A total of 118 VMC children were randomly and equally divided into routine treatment group and combined treatment group (received FDP therapy based on routine treatment), both groups were treated for two weeks. Therapeutic effect after treatment, levels of creatine kinase (CK), lactate dehydrogenase (LDH), CK isoenzyme MB (CK-MB), α-hydroxybutyrate dehydrogenase (HBDH), heart rate (HR), stroke volume (SV), cardiac output (CO) and left ventricular ejection fraction (LVEF) before and after treatment were measured and compared between two groups. Results: Total effective rate of combined treatment group was significantly higher than that of routine treatment group (91. 53％ vs. 71. 19％, P=0. 005). Compared with before treatment after two-week treatment, there were significant reductions in levels of CK, LDH, CK-MB, HBDH and HR, and significant rise in SV, CO and LVEF in two groups, P＜0. 01 all. Compared with routine treatment group after two-week treatment, there were significant reductions in levels of CK [(168. 2±33. 7) U/L vs. (126. 4±30. 4) U/L], LDH [(199. 0±41. 3) U/L vs. (162. 7±47. 1) U/L], CK-MB [(18. 3±6. 4) U/ L vs. (12. 2±6. 6) U/L], and HR [(85. 4±12. 6) times/min vs. (80. 2±12. 3) times/min], and significant rise in SV [(82. 4±13. 4) ml vs. (89. 5±14. 0) ml]and LVEF [(50. 1±8. 5) ％ vs. (59. 7±8. 8) ％]in combined treatment group, P＜0. 05 or＜0. 01. Conclusion: Fructose-1, 6-diphosphate combined antiviral therapy could significantly improve myocardial enzyme levels, recover cardiac pump function with significant therapeutic effect in VMC pediatric patients.
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Objective: To investigate the effects of leptin on the proliferation and apoptosis of human breast cancer BT-474 and MDA-MB-231 cells, and to explore its underlying molecular mechanism. Methods: After treatment with 200 ng/mL leptin, the proliferation and apoptosis of BT-474 and MDA-MB-231 cells were measured by CCK-8 assay and FCM, respectively; the expression levels of proliferation-and apoptosis-Associated proteins c-myc, cyclin D1, Bcl-2 and Bax were determined by Western blotting; while the levels of fructose-1, 6-bisphosphatase 1 (FBP1) mRNA and protein were detected by real-Time fluorescent quantitative PCR and Western blotting, respectively. After the recombinant plasmids carrying FBP 1 gene were transfected by liposome into BT-474 and MDA-MB-231 cells which were treated with 200 ng/mL leptin, the expression levels of FBP1 mRNA and protein were detected by real-Time fluorescent quantitative PCR and Western blotting to verify the over-expression of FBP 1 gene. Then, the proliferation abilities of BT-474 and MDA-MB-231 cells were measured by CCK-8 assay, the expression levels of proliferation-Associated proteins c-myc and cyclin D1 were determined by Western blotting, the apoptosis rates of the two cell lines were detected by FCM, and the expression levels of apoptosis-Associated proteins Bcl-2 and Bax were determined by Western blotting. Results: After treatment with 200 ng/mL leptin, the proliferation abilities of human breast cancer BT-474 and MDA-MB-231 cells were significantly increased (both P < 0.01); the expressions of proliferation-Associated proteins c-myc and cyclin D1 were significantly upregulated (both P < 0.01); while the apoptosis rates were apparently reduced (both P < 0.01); the expression of apoptosis-Associated protein Bcl-2 was apparently up-regulated (P < 0.01), but the expression of Bax was apparently down-regulated (P < 0.01); the mRNA and protein levels of FBP1 in BT-474 and MDA-MB-231 cells were obviously down-regulated (both P < 0.05). However, after transfection with FBP1 over-expression plasmids, the expressions of FBP1 mRNA and protein were significantly up-regulated in BT-474 and MDA-MB-231 cells (both P < 0.01), while the effects of leptin on proliferation and apoptosis of BT-474 and MDA-MB-231 cells were dramatically reversed (all P < 0.01). Conclusion: Leptin promotes the proliferation and inhibits the apoptosis of human breast cancer BT-474 and MDA-MB-231 cells, and the potential mechanism may be related to the down-regulation of FBP 1 gene expression.
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Objective: To investigate the effects of over-expressing fructose-1, 6-bisphosphatase 1 (FBP 1) gene on migration and apoptosis of tamoxifen-resistant MCF-7 human breast cancer cells. Methods: The levels of FBP1 mRNA and protein in human breast cancer tamoxifen-sensitive MCF-7 cells and tamoxifen-resistant MCF-7R cells were measured by real-time fluorescent quantitative PCR and Western blotting, respectively. Then, the FBP1 over-expression plasmids were transfected into MCF-7R cells by lipofectin, and the expression levels of FBP1 mRNA and protein were detected by real-time fluorescent quantitative PCR and Western blotting in order to verify the over-expression of FBP 1 gene. After that, the morphology of MCF-7R cells with FBP1 over-expression was observed under an inverted optical microscope, the abilities of cell migration and apoptosis were measured by cell wound healing experiment and FCM assay, respectively. Furthermore, the expressions of apoptosis-associated proteins Bcl-2 and Bax as well as the epithelial-mesenchymal transition (EMT) markers E-cadherin and vimentin were detected by Western blotting. Results: The mRNA and protein levels of FBP1 in human breast cancer tamoxifen-resistant MCF-7R cells were lower than those in tamoxifen-sensitive MCF-7 cells (both P< 0.01). After the transfection of FBP1 over-expression plasmids, the mRNA and protein expressions of FBP1 were significantly up-regulated in MCF-7R cells (both P< 0.01), MCF-7R cells had a change from mesenchymal-like morphology to epithelial-like morphology, the apoptotic index of MCF-7R cells was increased (P < 0.01), but the ability of cell migration was decreased (P < 0.01). Moreover, the protein expressions of Bcl-2 and vimentin were obviously down-regulated (both P<0.01), while the protein expressions of Bax and E-cadherin were significantly up-regulated (both P<0.01). Conclusion: The over-expression of FBP 1 gene can significantly inhibit cell migration and EMT in human breast cancer tamoxifen-resistant MCF-7R cells, and promote apoptosis through decreasing Bcl-2 expression and increasing Bax expression.
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Objetivos: revisar dados da literatura sobre isolamento de ilhotas pancreáticas para transplante e sobre as ações da frutose-1,6-bisfosfato. Fonte de dados: revisão de artigos publicados, a partir da pesquisa em bancos de dados nacionais e internacionais (SciELO, Lilacs, PubMed). Síntese dos dados: o transplante de ilhotas surge como uma alternativa para o tratamento do diabetes mellitus tipo 1. Entretanto, durante o processo de isolamento, há grande perda celular, principalmente na periferia da ilhota pancreática. As espécies reativas de oxigênio contribuem significativamente nesse processo, afetando a viabilidade das células para transplante. Vários esforços estão sendo feitos na tentativa de minimizar os danos causados pela liberação e produção destes compostos químicos. Conclusões: frente às importantes ações da frutose-1,6-bisfosfato descritas na literatura, seu emprego durante o processo de isolamento das ilhotas pancreáticas parece ser uma alternativa bastante atraente. O efeito da frutose-1,6-bisfosfato na redução da formação e liberação de radicais livres, assim como a sua ação citoprotetora, poderiam viabilizar um maior número de células, otimizando o processo de isolamento, além de auxiliar na enxertia, por diminuir a liberação de citocinas pró-inflamatórias.
Aims: To review the literature data about pancreatic islet isolation and fructose-1,6-bisphosfate. Source of data: Review of specific articles on the issue published in national and internacional databases (SciELO,Lilacs, PubMed). Summary of findings: Islets transplantation is an alternative for the treatment of type 1 diabetes mellitus. However, during the process of isolation, cell loss, mainly on the periphery of the pancreatic islet, ensues. Reactive oxygen species seem to contribute significantly in this process, affecting the viability of these cells. Various efforts are being made in an attempt to minimize the damage caused by the release and production of reactive oxygen species. Conclusions: Considering the important actions of fructose-1,6-bisphosphate which are described in the literature, its use in pancreatic islet isolation may represent an attractive alternative. The effect of fructose-1,6-bisphosphate in reducing the production and release of free radicals, as well as its role in cellular protection, could enable a greater number of viable cells, optimizing the isolation process, and also protecting the graft process, by reducing the release of proinflammatory cytokines.
Subject(s)
Humans , Male , Female , Diabetes Mellitus, Type 1 , Fructose-Bisphosphatase , Islets of Langerhans/growth & development , Islets of Langerhans TransplantationABSTRACT
Activity of fructose-1,6-bisphosphatase (EC 3.1.3.11), one of the key gluconeogenic enzymes, was measured in human fetal brain and liver during development. Fructose-1,6- bisphosphatase was distributed throughout the different regions of the brain. In contrast to the partially purified enzyme from the brain, the liver enzyme was dependent on Mg2+ for maximal activity, EDTA, citrate, oleate and linoleate were stimulatory, whereas 5'-AMP inhibited the activity of the liver enzyme.