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1.
Phytomedicine ; : 153498, 2021 Feb 12.
Artigo em Inglês | MEDLINE | ID: mdl-33640247

RESUMO

BACKGROUND: The incidence of nonalcoholic fatty liver disease (NAFLD), especially nonalcoholic steatohepatitis (NASH), has significantly increased in recent years and has become an important public health issue. However, no U.S. Food and Drug Administration (FDA)-approved first-line drug is currently available for the treatment of NAFLD and NASH; therefore, research on new drugs is currently a hot topic. Oroxylum indicum (Linn.) Kurz is extensively distributed in South China and South Asia and has many biological activities. However, its effects on NAFLD or even NASH and the corresponding mechanisms are still not clear. PURPOSE: To investigate the effect and mechanism of O. indicum seed extract (OISE) on preventing anti-inflammatory action in the progression from simple nonalcoholic fatty liver (NAFL) to NASH. METHODS: A network pharmacology method to construct ingredient-target networks and the protein-protein interaction (PPI) network of OISE in NASH were constructed for topological analyses and hub-target screening. Enrichment analyses were performed to identify the critical biological processes and signaling pathways. Simultaneously, in vitro and in vivo experiments investigated the effect and mechanism of OISE, baicalein, and chrysin on inflammation by biochemical indicator detection, luciferase reporters, pathological staining, and immunoblotting in oleic acid-stimulated HepG2 cells or in high-fat diet-fed rats. RESULTS: The network pharmacology showed that OISE prevented the development and progression of NAFL into NASH through various pathways and targets and that the nuclear factor NF-κB (NF-κB) pathway regulated by baicalein and chrysin played an important role in the treatment of NASH. In in vitro experiments, we further showed that OISE and its ingredients, namely, baicalein and chrysin, all improved the inflammatory status in oleic acid-stimulated HepG2 cells, inhibited the nuclear transcriptional activities of NF-κB, increased the IκB level, and decreased the phosphorylation level of NF-κB. Furthermore, in a high-fat diet-induced NASH model in rats, we also showed that OISE prevented the development and progression of NASH by inhibiting the nuclear transcriptional activity of NF-κB. CONCLUSION: OISE suppressed inflammatory responses and prevented the development and progression of NAFL into NASH through inhibition of the nuclear transcriptional activity of NF-κB. OISE may be used to treat NAFLD through many functions, including an increase in insulin sensitivity, a decrease in lipid accumulation in the liver, suppression of inflammation, and clearance of free radicals.

2.
J Agric Food Chem ; 68(39): 10489-10516, 2020 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-32846084

RESUMO

Caffeoylquinic acids (CQAs) are a broad class of secondary metabolites that have been found in edible and medicinal plants from various families. It has been 100 years since the discovery of chlorogenic acid in 1920. In recent years, a number of naturally derived CQAs have been isolated and structurally elucidated. Accumulated evidence demonstrate that CQAs have a wide range of biological activities, such as antioxidation, antibacterial, antiparasitic, neuroprotective, anti-inflammatory, anticancer, antiviral, and antidiabetic effects. Up to date, some meaningful progresses on the biosynthesis and total synthesis of CQAs have also been made. Therefore, it is necessary to comprehensively summarize the structure, biological activity, biosynthesis, and chemical synthesis of CQAs. This review provides extensive coverage of naturally occurring CQAs discovered from 1990 until 2020. Modern isolation techniques, chemical data (including structure, biosynthesis, and total synthesis), and bioactivity are summarized. This would be helpful for further research of CQAs as potential pharmaceutical agents.

4.
Food Funct ; 11(1): 711-721, 2020 Jan 29.
Artigo em Inglês | MEDLINE | ID: mdl-31909773

RESUMO

Nonalcoholic fatty liver disease (NAFLD) has become the most common liver disease worldwide; thus, a dietary supplement that can restrict hepatic fat accumulation is needed. Baicalein, a major component of Scutellaria baicalensis, is used as a dietary supplement in Eastern and Western cultures and can reduce hepatic fat accumulation. However, the detailed mechanism by which baicalein exerts this effect has yet to be elucidated in vivo and in vitro. In this study, we characterized the hepatic fat-lowering activity of baicalein and found that baicalein reduced hepatic fat accumulation by activating AMPK and suppressing SREBP1 cleavage, thus consequently inhibiting the transcriptional activity of SREBP1 and the synthesis of hepatic fat in oleic acid-induced HepG2 cells and high-fat diet-induced non-insulin-resistant mice. Moreover, baicalein improved NAFLD by decreasing TC, increasing HDLC, decreasing LDLC, affecting antioxidant activity, and exerting other effects. Therefore, the mechanism of baicalein with regard to NAFLD prevention and treatment might involve effects on multiple targets and pathways. Our study supports the use of baicalein as a dietary supplement due to its ability to reduce hepatic fat accumulation and to ameliorate NAFLD-related biochemical abnormalities.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Antioxidantes/farmacologia , Flavanonas/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/metabolismo , Proteína de Ligação a Elemento Regulador de Esterol 1/efeitos dos fármacos , Animais , Antioxidantes/administração & dosagem , Dieta Hiperlipídica , Flavanonas/administração & dosagem , Células Hep G2/metabolismo , Humanos , Técnicas In Vitro , Masculino , Camundongos , Camundongos Endogâmicos , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Ácido Oleico , Proteína de Ligação a Elemento Regulador de Esterol 1/metabolismo
5.
Life Sci ; 244: 117343, 2020 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-31978449

RESUMO

AIMS: Epithelial-mesenchymal transition (EMT) is one of the important regulators of metastasis in advanced hepatocellular carcinoma (HCC). Blocking the Notch signaling pathway and then reversing the EMT process is a hot spot in clinical tumor research. Here, we aimed to investigate the effect and underlying mechanisms of ADAM-17 (a key cleavage enzyme of Notch pathway) inhibitor ZLDI-8 we found before on the metastasis of hepatocellular carcinoma in vitro and in vivo. MAIN METHODS: The cell viability of HCC cells was evaluated by MTT and colony formation assays. Migration and invasion were assessed respectively with wound healing and transwell assays. The expression and location of proteins were detected by western blot and immunofluorescence, respectively. The effects of ZLDI-8 on metastasis of liver cancer in vivo were investigated in a tail vein injection model. KEY FINDINGS: In the present work, ZLDI-8 significantly inhibited proliferation, migration, invasion and EMT phenotype of highly aggressive MHCC97-H and LM3 cells. Moreover, ZLDI-8 could inhibit the migration and invasion of HepG2 and Bel7402 cells induced by TGF-ß1. ZLDI-8 suppressed the protein expression of interstitial markers and increased that of epithelial markers. Meanwhile, ZLDI-8 decreased the expression of proteins in the Notch signaling pathway. Finally, ZLDI-8 blocks metastasis in the lung metastasis model in vivo. SIGNIFICANCE: ZLDI-8 suppressed the metastasis of hepatocellular carcinoma, which was associated with reversing the EMT process and regulating Notch signaling pathway. The study laid the foundation for the discovery of drugs that reverse EMT to inhibit advanced HCC metastasis.


Assuntos
Proteína ADAM17/antagonistas & inibidores , Carcinoma Hepatocelular/tratamento farmacológico , Inibidores Enzimáticos/farmacologia , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Pulmonares/tratamento farmacológico , Animais , Apoptose , Carcinoma Hepatocelular/enzimologia , Carcinoma Hepatocelular/patologia , Proliferação de Células , Humanos , Técnicas In Vitro , Neoplasias Hepáticas/enzimologia , Neoplasias Hepáticas/patologia , Neoplasias Pulmonares/enzimologia , Neoplasias Pulmonares/secundário , Camundongos , Camundongos Nus , Transdução de Sinais , Células Tumorais Cultivadas , Ensaios Antitumorais Modelo de Xenoenxerto
6.
J Pak Med Assoc ; 68(11): 1644-11649, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30410143

RESUMO

OBJECTIVE: To investigate if lectin-like oxidised low density lipoprotein receptor is implicated in oxidised low density lipoprotein induced up regulation of tissue factor and whether recombinant domain V of beta (2)-Glycoprotein I expressed in Pichia pastoris inhibits the binding of oxidised and lectin-like low density lipoprotein. METHODS: The expression of tissue factor and lectin-like oxidised low density lipoprotein receptor was detected using Western blot methods. Small interference ribonucleic acid of lectin-like oxidised low density lipoprotein receptor was used to block lectin-like oxidised low density lipoprotein receptor expression. Flow cytometry was used to test the effect of beta (2)-Glycoprotein I expressed in Pichia pastoris on the binding of oxidised low density lipoprotein with lectin-like oxidised low density lipoprotein receptor by using the lectin-like oxidised low density lipoprotein receptor-expressing 293T cells. RESULTS: Oxidised low density lipoprotein at 5-10 g/mL increased tissue factor and lectin-like oxidised low density lipoprotein receptor expression, whereas 20-50 g/mL oxidised low density lipoprotein attenuated tissue factor expression. Inhibiting lectin-like oxidised low density lipoprotein receptor expression by small interference ribonucleic acid of lectin-like oxidised low density lipoprotein receptor impaired oxidised low density lipoprotein-induced tissue factor over expression in macrophages. Pretreatment with beta (2)-Glycoprotein I expressed in Pichia pastoris led to a strong inhibition of tissue factor and lectin-like oxidised low density lipoprotein receptor expression in a dose-dependent manner in macrophages. Flow cytometry analysis showed that beta (2)-Glycoprotein I expressed in Pichia pastoris attenuated the interaction of oxidised low density lipoprotein with lectin-like oxidised low density lipoprotein receptor in lectin-like oxidised low density lipoprotein receptor-expressing 293T cells. CONCLUSIONS: Lectin-like oxidised low density lipoprotein receptor was implicated in the expression of tissue factor induced by oxidised low density lipoprotein, and beta (2)-Glycoprotein I expressed in Pichia pastoris inhibited oxidised low density lipoprotein-induced tissue factor and lectin-like oxidised low density lipoprotein receptor expression, at least in part, via inhibition of the interaction between oxidised low density lipoprotein and lectin-like oxidised low density lipoprotein receptor.


Assuntos
Regulação da Expressão Gênica , Lipoproteínas LDL/metabolismo , Macrófagos/metabolismo , Tromboplastina/biossíntese , beta 2-Glicoproteína I/metabolismo , Animais , Western Blotting , Camundongos , Oxirredução , Coelhos
7.
Sheng Wu Gong Cheng Xue Bao ; 34(1): 110-121, 2018 Jan 25.
Artigo em Chinês | MEDLINE | ID: mdl-29380576

RESUMO

CD36, the major scavenger receptor, is intimately involved in the uptake of oxLDL in macrophages. To further study the function of CD36 in macrophages, we constructed CD36 gene silence cell lines (J774A.1) by lentivirus-mediated RNA interference technique, and analyzed the effect of CD36 in caveolin-1 protein expression. At first, 5 shRNA fragments were designed and synthesized according to the coding sequence (CDS) region of CD36 gene. Next, the CD36-shRNA was inserted into lentiviral vector to yield pLKO.1-CD36-shRNA plasmid. After DNA sequencing, the pLKO.1-CD36-shRNA plasmid and psiCHECK-II-CD36 were co-transfected into the 293T cells to screen the efficient CD36-shRNA. The efficient CD36-shRNA plasmid and the helper plasmid were co-transfected into the 293T cells to package the lentivirus, and then infected the J774A.1 cells. After screening by puromycin, CD36 gene silence cell lines (J774A.1) was established. Western blotting and confocal fluorescence microscopy results showed that the CD36 silencing efficiency in the gene silence cell line was 90%. Accompanied by a decrease in CD36 protein on cell surface, oxLDL binding to CD36 was significantly inhibited, indicating that the CD36 gene silence cell line is successfully established. Finally, the oxLDL stimulation and inhibitor experiments results showed that the CD36 knockdown significantly suppresses the phosphorylation of JNK and ERK, thereby inhibiting the oxLDL-induced caveolin-1 protein expression, demonstrating that CD36 modulates the caveolin-1 protein expression through the JNK/ERK-mediated signaling transduction.


Assuntos
Antígenos CD36/genética , Caveolina 1/metabolismo , Lentivirus , Interferência de RNA , Animais , Linhagem Celular , Vetores Genéticos , Camundongos , RNA Interferente Pequeno , Transdução de Sinais
8.
Life Sci ; 192: 270-277, 2018 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-29129771

RESUMO

Tumor metastasis leads to a poor prognosis in breast cancer, yet the mechanisms remain unclear. Docosahexaenoic acid (DHA) extracted from Antarctic krill is an optical isomer of common DHA and has a much stronger anti-neoplastic effect. In this work, the migration and invasion abilities of MCF-7 cells treated with low concentrations of Antarctic krill DHA were evaluated. Low concentrations of Antarctic krill DHA significantly reduced the numbers of migrating and invasive MCF-7 cells, whereas the cell numbers decreased slowly in the CD95-silenced MCF-7 cells, which implies that CD95 might be involved in cell migration and invasion. Additionally, co-immunoprecipitation and Western blotting demonstrated that Antarctic krill DHA induced the accumulation of CD95 and caveolin-1 interaction, resulting in the down-regulation of MMP2 expression through the FAK/SRC/PI3K/AKT signaling pathway. In conclusion, Antarctic krill DHA enhanced the interaction between CD95 and caveolin-1, which may led to an inhibitory effect on cell migration and invasion via the FAK/SRC/PI3K/AKT signaling pathway. Our study indicates that Antarctic krill DHA has great potential for tumor therapy and has revealed a new metastatic mechanism mediated by the interaction of CD95 with caveolin-1.


Assuntos
Caveolina 1/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Ácidos Docosa-Hexaenoicos/farmacologia , Euphausiacea/química , Invasividade Neoplásica , Receptor fas/efeitos dos fármacos , Animais , Regiões Antárticas , Contagem de Células , Sobrevivência Celular , Feminino , Humanos , Células MCF-7 , Metaloproteinase 2 da Matriz/biossíntese , Metaloproteinase 2 da Matriz/genética , Metástase Neoplásica , Transdução de Sinais/efeitos dos fármacos
9.
Sheng Wu Gong Cheng Xue Bao ; 33(1): 122-131, 2017 Jan 25.
Artigo em Chinês | MEDLINE | ID: mdl-28959869

RESUMO

We analyzed the binding of P.rß2-GPI-DV with ox-LDL by fluorescence, molecular simulation and circular dichroism. We used SDS-PAGE and Western blotting to identify the purity of P.rß2-GPI-DV, fluorescence, circular dichroism spectroscopy and molecular docking simulation to analyze the binding between P.rß2-GPI-DV and oxLDL. P.rß2-GPI-DV was specifically recognized by anti-His antibody at 12 kDa position. The chromophoric groups, the changes of secondary structure and the molecular docking simulations revealed that the active pocket formed by Cys281-Lys-Asn-Lys-Glu-Lys-Lys287 and Leu313-Ala-Phe-Trp316 of P.rß2-GPI-DV and the -COOH carboxyl of oxLig-1 were the key for binding. P.rß2-GPI combined with ox-LDL via the fifth functional domain and the -COOH group. Our findings provide theoretical basis to further study the binding between ß2-GPI and ox-LDL in serum.


Assuntos
Lipoproteínas LDL/metabolismo , Simulação de Acoplamento Molecular , beta 2-Glicoproteína I/metabolismo , Anticorpos , Western Blotting , Ésteres do Colesterol , Dipeptídeos , Eletroforese em Gel de Poliacrilamida , Glicoproteínas , Humanos
10.
Int J Biochem Cell Biol ; 90: 121-135, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28789920

RESUMO

CD36 signal transduction modulates the uptake of oxidized low-density lipoprotein (oxLDL) and foam cell formation. We previously observed that 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), the lipid moiety of oxLDL, activates the CD36-Src-JNK/ERK1/2 signalling pathway. In this study, we assessed the role of the ω-carboxyl group in the binding of oxLig-1 to CD36 and investigated whether the binding of the ω-carboxyl group to CD36 triggers CD36-mediated signalling, thereby resulting in the upregulation of caveolin-1 expression. Our results showed that oxLig-1 bound to CD36 and that the ω-carboxyl group was critical for this binding. Furthermore, immunoprecipitation and Western blot analyses showed that interaction between the ω-carboxyl group of oxLig-1 and CD36 triggered intracellular Src-JNK/ERK1/2 signal transduction. Moreover, the binding of the ω-carboxyl group to CD36 induced caveolin-1 expression and translocation to the membrane in macrophages. Additionally, inhibitors of Src, JNK and ERK and siRNA targeting CD36 and NF-κB significantly suppressed the enhanced caveolin-1 expression induced by oxLig-1. In conclusion, these observations suggest that oxLig-1 is a critical epitope of oxLDL that mediates the binding of oxLDL to CD36 and activates downstream Src-JNK/ERK1/2-NF-κB signal transduction, resulting in upregulation of caveolin-1 expression in macrophages.


Assuntos
Antígenos CD36/metabolismo , Caveolina 1/metabolismo , Ésteres do Colesterol/química , Ésteres do Colesterol/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Lipoproteínas LDL/metabolismo , Macrófagos/efeitos dos fármacos , Antígenos CD36/química , Linhagem Celular , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Humanos , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Lipoproteínas LDL/química , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Macrófagos/citologia , Macrófagos/metabolismo , Simulação de Acoplamento Molecular , NF-kappa B/metabolismo , Ligação Proteica/efeitos dos fármacos , Conformação Proteica , Transporte Proteico/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-fyn/metabolismo , Relação Estrutura-Atividade
11.
Life Sci ; 177: 27-40, 2017 May 15.
Artigo em Inglês | MEDLINE | ID: mdl-28377266

RESUMO

AIM: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1), a specific membrane receptor for oxidized low-density lipoprotein (oxLDL), plays a crucial role in atherosclerosis progression. The aim of this study was to elucidate the role of 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), a lipid component of oxLDL, in the binding of oxLDL to LOX-1 and to determine whether oxLig-1 binding to LOX-1 is involved in the upregulation of ABCA1 expression. MAIN METHODS: OxLig-1 binding to LOX-1 was analysed by AutoDock 4.2.6 and confirmed by fluorescence immunocytochemistry and enzyme-linked immunosorbent assays (ELISAs). LOX-1, LXRα and ABCA1 protein expression induced by oxLig-1 or methylated oxLig-1 was measured by western blotting. In addition, PPARγ activation was investigated using a dual-luciferase reporter system. Furthermore, the signalling cascade involved in oxLig-1-induced ABCA1 expression was assessed using inhibitors for PPARγ and LXRα and specific siRNAs against LOX-1, PPARγ and LXRα. KEY FINDINGS: Docking, fluorescence immunocytochemistry and ELISA analyses showed that oxLig-1 bound LOX-1 and that the ω-carboxyl group was critical for this binding. Moreover, oxLig-1, but not methylated oxLig-1, increased LOX-1, LXRα, and ABCA1 expression. Luciferase reporter assays indicated that oxLig-1 activated PPARγ in the presence of LOX-1. Additionally, the inhibitor and siRNA experiments showed that oxLig-1 triggered the PPARγ-LXRα signalling pathway, leading to upregulation of ABCA1, and that this process required the participation of LOX-1. SIGNIFICANCE: Our observations indicate that oxLig-1 is a critical epitope of oxLDL that mediates the binding of oxLDL to LOX-1 and initiates PPARγ signal transduction to upregulate the expression of ABCA1.


Assuntos
Transportador 1 de Cassete de Ligação de ATP/genética , Ésteres do Colesterol/metabolismo , Lipoproteínas LDL/metabolismo , PPAR gama/metabolismo , Receptores Depuradores Classe E/metabolismo , Animais , Western Blotting , Linhagem Celular , Ensaio de Imunoadsorção Enzimática , Epitopos , Humanos , Camundongos , Simulação de Acoplamento Molecular , Transdução de Sinais , Regulação para Cima
12.
J Clin Immunol ; 34(6): 669-76, 2014 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-24970589

RESUMO

ß2-glycoprotein I (ß2-GPI) is a plasma protein that interacts with oxidized low-density lipoproteins (oxLDL) via ß2-GPI domain V to form oxLDL/ß2-GPI complexes, potential autoantigens promoting atherogenesis in patients with antiphospholipid syndrome (APS). Such a interaction would expose ß2-GPI domain I or/and IV, structures recognized by anti-ß2-GPI autoantibodies. IgG immune complexes with oxLDL/ß2-GPI complexes can interact with macrophages via Fcγ receptor, causing oxLDL/ß2-GPI endocytosis and foam cell formation, contributing to atherosclerosis. Here, we use recombinant domain V to study the interaction between oxLDL and ß2-GPI and hypothesized that domain V would interfere with this interaction thereby reducing oxLDL macrophage uptake and foam cell formation. The ß2-GPI domain V sequence was expressed by using the Pichia pastoris expression system to obtain recombinant domain V of ß2-GPI (P.rß2-GPI DV). ELISA tests demonstrated that P.rß2-GPI DV interacted with oxLDL via 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), a negatively charged lipid moiety of oxLDL. The ω-carboxyl residue of oxLig-1 is required for the interaction. Serologic tests showed a significant increase in oxLDL and oxLDL/ß2-GPI levels in patients with APS (p < 0.05 compared to controls). P.rß2-GPI DV was able to bind oxLDL in high affinity and competitively inhibited native ß2-GPI (nß2-GPI) binding to free oxLDL as well as to oxLDL from the oxLDL/ß2-GPI complexes. These observations suggest that P.rß2-GPI DV may be used to inhibit the formation of the oxLDL/ß2-GPI complexes, a potential approach for reducing foam cell development and mitigating atherogenesis in patients with APS. The present work provides a new effective strategy to prevent the progression of atherothrombotic vascular complications in APS patients.


Assuntos
Complexo Antígeno-Anticorpo/metabolismo , Síndrome Antifosfolipídica/tratamento farmacológico , Autoantígenos/metabolismo , Células Espumosas/fisiologia , Lipoproteínas LDL/metabolismo , Placa Aterosclerótica/prevenção & controle , beta 2-Glicoproteína I/metabolismo , Complexo Antígeno-Anticorpo/imunologia , Síndrome Antifosfolipídica/complicações , Aterosclerose , Autoanticorpos/imunologia , Autoanticorpos/metabolismo , Autoantígenos/imunologia , Ésteres do Colesterol/metabolismo , Endocitose , Humanos , Placa Aterosclerótica/etiologia , Ligação Proteica , Estrutura Terciária de Proteína/genética , Proteínas Recombinantes/genética , beta 2-Glicoproteína I/genética
13.
Atherosclerosis ; 226(1): 102-9, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-23200840

RESUMO

BACKGROUND: CD36 signal transductions have been reported by a variety of lipid moiety of oxidized low-density lipoprotein (oxLDL), however, CD36 signal induced by 7-ketocholesteryl-9-carboxynonanoate (oxLig-1), a lipid moiety of oxLDL has not been elucidated. METHODS AND RESULTS: OxLig-1 leads to activation and recruitment of Src kinase Fyn, Lyn and caveolin-1 to CD36 in J774A.1 cells, but not in CD36 knockdown cells. The mitogen-activated protein (MAP) kinases c-Jun N-terminal kinase 2 (JNK2) and extracellular signal-regulated protein kinase 1 and 2 (ERK1/2) are specifically phosphorylated in J774A.1 cells after treatment with oxLig-1 and inhibited by pretreatment of Src inhibitor, AG1879. The expression of ABCA1 is up-regulated by treatment with oxLig-1in J774A.1 cells, and the increased expression of ABCA1 is dramatically down-regulated by pretreatment with pharmacological inhibitors of ERK (PD98059) and JNK (SP600125). CONCLUSIONS: The specific CD36 signal induced by oxLig-1 initiated the activation of Fyn, Lyn, caveolin-1, JNK2 and ERK1/2, and resulted in the up-regulation of ABCA1.


Assuntos
Transportadores de Cassetes de Ligação de ATP/biossíntese , Transportadores de Cassetes de Ligação de ATP/efeitos dos fármacos , Antígenos CD36/fisiologia , Ésteres do Colesterol/farmacologia , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Transportador 1 de Cassete de Ligação de ATP
14.
J Hazard Mater ; 172(1): 408-15, 2009 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-19660862

RESUMO

Advanced treatment of mature landfill leachate from a municipal landfill located in southern China (Jiangmen) was carried out in a full-scale plant using a new process. The combined process has a sequencing batch reactor (SBR) serving as the primary treatment, with polyferric sulfate (PFS) coagulation coupled with a Fenton system as secondary treatment, and a pair of upflow biological aerated filters (UBAFs) in parallel as tertiary treatment. The overall removal efficiency of chemical oxygen demand (COD) in this process was 97.3%, with an effluent COD less than 100 mg/L. Up to 99% ammonia (N-NH3) removal efficiency was achieved in the SBR, with an effluent of less than 3 mg/L, which meets the discharge standard (< or =25 mg/L) with only primary treatment. The total phosphorus (TP) and suspended solids (SS) in the final effluent were reduced to less than 1 mg/L and 10 mg/L, respectively. The experience gained in the operation and maintenance will lead to a more stable performance of this combined process. An economic analysis shows that the overall operating cost of the advanced treatment was $2.70/m(3). This new combination process was proved to be highly compatible and efficient in a small-scale landfill leachate treatment plant and is recommended for small-scale landfill leachate treatment plants.


Assuntos
Eliminação de Resíduos/métodos , Purificação da Água/métodos , Aerobiose , Amônia/química , Biodegradação Ambiental , Reatores Biológicos , China , Desenho de Equipamento , Peróxido de Hidrogênio/química , Concentração de Íons de Hidrogênio , Ferro/química , Oxigênio/química , Fósforo/química , Compostos de Amônio Quaternário/química , Eliminação de Resíduos/economia , Sulfatos/química , Poluentes Químicos da Água/isolamento & purificação , Purificação da Água/economia
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