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1.
Front Pharmacol ; 12: 703965, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34557092

RESUMO

Xiaoyaosan (XYS), as a classic Chinese medicine compound, has been proven to have antidepressant effect in many studies, but its mechanism has not been clarified. In our previous studies, we found that chronic stress can induce depressive-like behavior and lead to emotion-related cingulate gyrus (Cg) dysfunction, as well as the decrease of neurotrophic factors and the increase of inflammatory-related proteins. Therefore, we speculated that XYS may play an antidepressant role by regulating the inflammation-related receptor of advanced glycation protein end product (RAGE) to affect the functional connectivity (FC) signal of the Cg and improve the depressive-like behavior. In order to verify this hypothesis, we analyzed the FC and RAGE expression in the Cg of depressive-like mice induced by chronic unpredictable mild stress (CUMS) and verified it with RAGE knockout mice. At the same time, we detected the effect of XYS on the depressive-like behavior, expression of RAGE, and the FC of the Cg of mice. The results showed that the FC of the Cg of depressive-like mice induced by CUMS was weakened, and the expression of RAGE was upregulated. The antidepressant effect of XYS is similar to that of fluoxetine hydrochloride, which can significantly reduce the depressive-like behavior of mice and inhibit the expression of the RAGE protein and mRNA in the Cg, and increase the FC of the Cg in mice. In conclusion, XYS may play an antidepressant role by downregulating the expression of RAGE in the Cg of depressive-like mice induced by CUMS, thereby affecting the functional signal and improving the depressive-like behavior.

3.
Chin J Integr Med ; 2021 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-34105096

RESUMO

OBJECTIVE: To investigate the molecular mechanism underlying the anti-hepatic fibrosis activity of ethyl acetate fraction Dicliptera chinensis (L.) Juss. (EDC) in human hepatic stellate cells (HSCs) in vitro and in a carbon tetrachloride (CCl4)-induced hepatic fibrosis mouse model in vivo. METHODS: For in vitro study, HSCs were pre-treated with platelet-derived growth factor (10 ng/mL) for 2 h to ensure activation and treated with EDC for 24 h and 48 h, respectively. The effect of EDC on HSCs was assessed using cell counting kit-8 assay, EdU staining, transmission electron microscopy, immunofluorescence staining, and Western blot, respectively. For in vivo experiments, mice were intraperitoneally injected with CCl4 (2 ° L/g, adjusted to a 25% concentration in olive oil), 3 times per week for 6 weeks, to develop a hepatic fibrosis model. Forty 8-week-old male C57BL/6 mice were divided into 4 groups using a random number table (n=10), including control, model, positive control and EDC treatment groups. Mice in the EDC and colchicine groups were intragastrically administered EDC (0.5 g/kg) or colchicine (0.2 mg/kg) once per day for 6 weeks. Mice in the control and model groups received an equal volume of saline. Biochemical assays and histological examinations were used to assess liver damage. Protein expression levels of α -smooth muscle actin (α -SMA) and microtubule-associated protein light chain 3B (LC3B) were measured by Western blot. RESULTS: EDC reduced pathological damage associated with liver fibrosis, downregulated the expression of α -SMA and upregulated the expression of LC3B (P<0.05), both in HSCs and the CCl4-induced liver fibrosis mouse model. The intervention of bafilomycin A1 and rapamycin in HSCs strongly supported the notion that inhibition of autophagy enhanced α -SMA protein expression levels (P<0.01). The results also found that the levels of phosphoinositide (PI3K), p-PI3K, AKT, p-AKT, mammalian target of rapamycin (mTOR), p-mTOR, and p-p70S6K all decreased after EDC treatment (P<0.05). CONCLUSIONS: EDC has anti-hepatic fibrosis activity by inducing autophagy and might be a potential drug to be further developed for human liver fibrosis therapy.

4.
Phytomedicine ; 84: 153524, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33667840

RESUMO

BACKGROUND: Indoleamine 2,3-dioxygenase 1 (IDO1) has been reported as a hallmark of hepatic fibrosis. Ginseng Rg1(G-Rg1) is a characterized bioactive component isolated from a traditional Chinese medicinal herb Panax ginseng C. A. Meyer (Ginseng) that used in China widely. However, the anti-hepatic fibrosis property of G-Rg1 and the underlying mechanisms of action are poorly reported. PURPOSE: Here, we researched the effect of G-Rg1 on experimental liver fibrosis in vivo and in vitro. STUDY DESIGN AND METHODS: We applied a CCL4-induced liver fibrosis in mice (wild-type and those overexpressing IDO1 by in vivo AAV9 vector) and HSC-T6 cells to detect the anti-hepatic fibrosis effect of G-Rg1 in vivo and in vitro. RESULTS: We found that G-Rg1 reduced serum levels of AST and ALT markedly. Histologic examination indicated that G-Rg1 dramatically improved the extent of liver fibrosis and suppressed the hepatic levels of fibrotic marker α-SMA in vivo and in vitro. The proliferation of HSC-T6 was significantly inhibited by G-Rg1 in vitro. Both TUNEL staining and flow cytometry demonstrated that G-Rg1 attenuated the levels of hepatocyte apoptosis in fibrotic mice. Additionally, G-Rg1 up-regulated the maturation of hepatic DCs via reducing the expression level of hepatic IDO1, which played an inverse role in the maturation of DCs. Furthermore, oral administration of G-Rg1 ameliorated IDO1 overexpression-induced worsen liver fibrosis as well as IDO1 overexpression-mediated more apparent inhibition of maturation of DCs. CONCLUSION: These results suggest that G-Rg1, which exerts its antifibrotic properties via alleviating IDO1-mediated the inhibition of DCs maturation, may be a potential therapeutic drug in treating liver fibrosis.


Assuntos
Células Dendríticas/efeitos dos fármacos , Inibidores Enzimáticos/farmacologia , Ginsenosídeos/farmacologia , Indolamina-Pirrol 2,3,-Dioxigenase/antagonistas & inibidores , Cirrose Hepática/prevenção & controle , Actinas/metabolismo , Animais , Células Dendríticas/fisiologia , Células Estreladas do Fígado/efeitos dos fármacos , Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo , Cirrose Hepática/induzido quimicamente , Cirrose Hepática/metabolismo , Cirrose Hepática/patologia , Masculino , Camundongos Endogâmicos C57BL , Panax/química , Substâncias Protetoras/farmacologia , Ratos
5.
Front Pharmacol ; 12: 616409, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33716743

RESUMO

Alcoholic liver disease (ALD) has become a heavy burden on health worldwide. Ginsenoside Rb1 (GRb1), extracted from Panax quinquefolium L., has protective effects on many diseases, but the effect and mechanisms of GRb1 on ALD remain unknown. This study aimed to investigate the protective effects of GRb1 on ALD and to discover the potential mechanisms. Zebrafish larvae were exposed to 350 mM ethanol for 32 h to establish a model of acute alcoholic liver injury, and the larvae were then treated with 6.25, 12.5, or 25 µM GRb1 for 48 h. The human hepatocyte cell line was stimulated by 100 mM ethanol and meanwhile incubated with 6.25, 12.5, and 25 µM GRb1 for 24 h. The lipid changes were detected by Oil Red O staining, Nile Red staining, and triglyceride determination. The antioxidant capacity was assessed by fluorescent probes in vivo, and the expression levels of inflammatory cytokines were detected by immunohistochemistry, immunofluorescence, and quantitative real-time PCR. The results showed that GRb1 alleviated lipid deposition in hepatocytes at an optimal concentration of 12.5 µM in vivo. GRb1 reversed the reactive oxygen species accumulation caused by alcohol consumption and partially restored the level of glutathione. Furthermore, GRb1 ameliorated liver inflammation by inhibiting neutrophil infiltration in the liver parenchyma and downregulating the expression of nuclear factor-kappa B pathway-associated proinflammatory cytokines, including tumor necrosis factor-α and interleukin-1ß. This study revealed that GRb1 has a protective effect on alcohol-induced liver injury due to its resistance to lipid deposition as well as antioxidant and anti-inflammatory actions. These findings suggest that GRb1 may be a promising candidate against ALD.

6.
Aging (Albany NY) ; 13(5): 6592-6605, 2021 03 11.
Artigo em Inglês | MEDLINE | ID: mdl-33707345

RESUMO

Acute hepatic damage is a severe condition characterized by inflammation and oxidative stress, which is a serious threat to people's life and health. But there are few effective treatments for acute liver injury. Therefore, safe and effective therapeutic approaches for preventing acute liver damage are urgently needed. Lupeol is a natural compound, which has significant antioxidant and anti-inflammatory properties in liver disease. However, the protective mechanism of lupeol against acute liver injury remains unclear. Here, zebrafish and mutant mice were utilized to investigate the protective effects of lupeol against lipopolysaccharide (LPS)/ D-galactosamine(D-GalN) -induced liver injury and the underlying mechanisms. We found that pretreatment with lupeol attenuated the LPS/D-GalN-induced liver injury by decreasing the infiltration of inflammatory cells and reducing pro-inflammatory cytokines. We also demonstrated that lupeol could protect injured liver from oxidative stress by downregulating the expression of TGFß1 and upregulating Nrf2. Notably, our experimental results provided the support that lupeol effectively protected against LPS/D-GalN-induced acute liver injury via suppression of inflammation response and oxidative stress, which were largely dependent on the upregulation of the Nrf2 pathway via downregulating TGFß1.


Assuntos
Anti-Inflamatórios/farmacologia , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Fator 2 Relacionado a NF-E2/metabolismo , Triterpenos Pentacíclicos/farmacologia , Fator de Crescimento Transformador beta1/metabolismo , Animais , Modelos Animais de Doenças , Regulação para Baixo , Galactosamina/toxicidade , Inflamação/prevenção & controle , Lipopolissacarídeos/toxicidade , Camundongos Endogâmicos C57BL , Estresse Oxidativo/efeitos dos fármacos , Regulação para Cima , Peixe-Zebra
7.
Cell Death Dis ; 12(1): 16, 2021 01 07.
Artigo em Inglês | MEDLINE | ID: mdl-33414436

RESUMO

Liver fibrosis is a course of chronic liver dysfunction, can develop into cirrhosis and hepatocellular carcinoma. Inflammatory insult owing to pathogenic factors plays a crucial role in the pathogenesis of liver fibrosis. Indoleamine 2,3-dioxygenase 1 (IDO1) can affect the infiltration of immune cells in many pathology processes of diseases, but its role in liver fibrosis has not been elucidated completely. Here, the markedly elevated protein IDO1 in livers was identified, and dendritic cells (DCs) immune-phenotypes were significantly altered after BDL challenge. A distinct hepatic population of CD11c+DCs was decreased and presented an immature immune-phenotype, reflected by lower expression levels of co-stimulatory molecules (CD40, MHCII). Frequencies of CD11c+CD80+, CD11c+CD86+, CD11c+MHCII+, and CD11c+CD40+ cells in splenic leukocytes were reduced significantly. Notably, IDO1 overexpression inhibited hepatic, splenic CD11c+DCs maturation, mature DCs-mediated T-cell proliferation and worsened liver fibrosis, whereas above pathological phenomena were reversed in IDO1-/- mice. Our data demonstrate that IDO1 affects the process of immune cells recruitment via inhibiting DCs maturation and subsequent T cells proliferation, resulting in the promotion of hepatic fibrosis. Thus, amelioration of immune responses in hepatic and splenic microenvironment by targeting IDO1 might be essential for the therapeutic effects on liver fibrosis.


Assuntos
Indolamina-Pirrol 2,3,-Dioxigenase/metabolismo , Cirrose Hepática/enzimologia , Cirrose Hepática/patologia , Animais , Ductos Biliares/enzimologia , Ductos Biliares/patologia , Ductos Biliares/cirurgia , Diferenciação Celular/fisiologia , Hepatócitos/enzimologia , Hepatócitos/metabolismo , Hepatócitos/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout
8.
Free Radic Biol Med ; 160: 178-190, 2020 11 20.
Artigo em Inglês | MEDLINE | ID: mdl-32771520

RESUMO

Liver fibrosis can develop into liver cirrhosis and hepatocellular carcinoma substantially without effective available treatment currently due to rarely characterized molecular pathogenesis. Indoleamine 2,3-dioxygenase 1(IDO1) can be detected on antigen-presenting cells (APCs) and modulates various immune responses. However, the role of IDO1 in the regulation of dendritic cells (DCs) during liver fibrosis is rarely reported. Here, we found that hepatic IDO1 was up-regulated during CCL4-induced liver fibrosis, which accompanied by a significant decrease in the frequencies of CD11c+CD80+, CD11c+CD86+, CD11c+CD40+ and CD11c+MHCII+ cells and a reduction in the subsequent T cell proliferation rate, whereas these changes were reversed significantly in IDO1-/- mice. Overexpressing IDO1 by adeno-associated viral vector serotype 9 (AAV9) significantly inhibited the maturation status of DCs, worsened fibrosis. In vitro studies showed that significantly elevated CD80, CD86, CD40 and MHCII expression were observed in BMDCs derived from IDO1-/- mice. Moreover, the maturation of BMDCs derived from WT mice were significantly increased after stimulated with IDO1 inhibitor (1-methyl- D -tryptophan). Nuclear factor E2-related factor 2 (Nrf2), a key regulator of the cellular adaptive response to oxidative insults and inflammation, exhibited a markedly decrease in the liver of WT fibrotic mice, nevertheless, knockout of IDO1 enhanced the protein level of Nrf2. Moreover, the expression of IDO1 and Nrf2 exhibited inverse colocalization pattern suggesting that ectopically expressed IDO1 down-regulated Nrf2. Additionally, up-regulation of IDO1 was also observed in the livers of Nrf2-/- fibrotic mice. Taken together, these data uncovered mutual antagonism between IDO1 and Nrf2 on the maturation status of DCs during hepatic fibrosis.


Assuntos
Indolamina-Pirrol 2,3,-Dioxigenase , Cirrose Hepática , Fator 2 Relacionado a NF-E2 , Animais , Células Dendríticas , Indolamina-Pirrol 2,3,-Dioxigenase/genética , Cirrose Hepática/genética , Camundongos , Fator 2 Relacionado a NF-E2/genética , Triptofano
9.
Free Radic Biol Med ; 152: 668-679, 2020 05 20.
Artigo em Inglês | MEDLINE | ID: mdl-31945497

RESUMO

Ferroptosis is a recently recognized form of regulated cell death that is characterized by lipid peroxidation. However, the molecular mechanisms of ferroptosis in acute immune hepatitis (AIH) are largely unknown. In this study, we investigated the classical ferroptotic events in the livers of mice with concanavalin A (ConA) to induce AIH. The dramatically upregulated gene indoleamine 2, 3-dioxygenase 1 (IDO1) was identified with AIH, and its role in generation of ferroptosis and reactive nitrogen species (RNS) was assessed both in vitro and in vivo by genetic deletion or pharmacologic inhibition of IDO1. We observed that ferroptosis contributed to the ConA-induced hepatic damage, which was confirmed by the therapeutical effects of ferroptosis inhibitor (ferrostatin-1). Noteworthy, upregulation of hepatic IDO1 and nitrative stress in ConA-induced hepatic damage were also remarkably inhibited by the ferroptosis abolishment. Additionally, IDO1 deficiency contributed to ferroptosis resistance by activating solute carrier family 7 member 11 (SLC7A11; also known as xCT) expression, accompanied with the reductions of murine liver lesions and RNS. Meanwhile, IDO inhibitor 1-methyl tryptophan alleviated murine liver damage with the reduction of inducible nitric oxide synthase and 3-nitrotyrosine expression. Consistent with the results in vivo, hepatocytes-specific knockdown of IDO1 led to ferroptosis resistance upon exposure to ferroptosis-inducing compound (Erastin) in vitro, whereas IDO1 overexpression aggravated the classical ferroptotic events, and the RNS stress. Overall, these results revealed a novel molecular mechanism of ferroptosis with the key feature of nitrative stress in ConA-induced liver injury, and also identified IDO1-dependent ferroptosis as a potential target for the treatment of AIH.


Assuntos
Ferroptose , Hepatite , Animais , Hepatócitos , Indolamina-Pirrol 2,3,-Dioxigenase/genética , Camundongos
10.
Sci Rep ; 9(1): 3666, 2019 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-30842464

RESUMO

The illuminated current-voltage characteristics of Cu(In,Ga)(S,Se)2 (CIGSSe) thin film solar cells fabricated using two different buffer layer processes: chemical bath deposition (CBD) and atomic layer deposition (ALD) were investigated. The CIGSSe solar cell with the ALD buffer showed comparable conversion efficiency to the CIGSSe solar cell with CBD buffer but lower shunt resistance even though it showed lower point shunt defect density as measured in electroluminescence. The shunt paths were investigated in detail by capturing the high-resolution dark lock-in thermography images, resolving the shunt resistance contributions of the scribing patterns (P1, P3), and depth profiling of the constituent elements. It was found that the concentration of Na from the soda-lime glass substrate played a key role in controlling the shunt paths. In the ALD process, Na segregated at the surface of CIGSSe and contributed to the increase in the shunt current through P1 and P3, resulting in a reduction in the fill factor of the CIGSSe solar cells.

11.
Front Pharmacol ; 10: 1594, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-32047433

RESUMO

Alcoholic liver disease (ALD), which is recognized as an important health problem worldwide, is a direct consequence of alcohol consumption, which can induce alcoholic fatty liver, alcoholic steatohepatitis, fibrosis and cirrhosis. P-Hydroxyacetophenone (p-HAP) is mainly used as a choleretic and hepatoprotective compound and has anti-hepatitis B, antioxidative and anti-inflammatory effects. However, no experimental report has focused on p-HAP in ALD, and the effect and mechanism of p-HAP in ALD remain unknown. In addition, there is no research on p-HAP in the treatment of ALD. The potential molecular mechanisms of p-HAP against acute alcoholic liver injury remain unknown. In this study, we aimed to investigate whether p-HAP alleviates ALD and to clarify the potential molecular mechanisms. Zebrafish larvae were soaked in 350 mmol/l ethanol for 32 h at 4 days post fertilization (dpf) and then treated with p-HAP for 48 h. We chose various outcome measures, such as liver histomorphological changes, antioxidation and antiapoptosis capability and expression of inflammation-related proteins, to elucidate the essential mechanism of p-HAP in the treatment of alcohol-induced liver damage. Subsequently, we applied pathological hematoxylin and eosin (H&E) staining, Nile red staining and oil red O staining to detect the histomorphological and lipid changes in liver tissues. We also used TUNEL staining, immunochemistry and Western blot analysis to reveal the changes in apoptosis- and inflammation-related proteins. In particular, we used a variety of fluorescent probes to detect the antioxidant capacity of p-HAP in live zebrafish larvae in vivo. In addition, we discovered that p-HAP treatment relieved alcoholic hepatic steatosis in a dose-dependent manner and that the 50 µM dose had the best therapeutic effect. Generally, this research indicated that p-HAP might reduce oxidative stress and cell apoptosis in vivo and in vitro via the NF-κB signaling pathway.

12.
Life Sci ; 216: 305-312, 2019 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-30031061

RESUMO

AIMS: Alcoholic liver disease (ALD) is a leading health risk worldwide, which can induce hepatic steatosis, progressive fibrosis, cirrhosis and even carcinoma. As a potential therapeutic drug for ALD, naringin, an abundant flavanone in grapefruit, could improve resistance to oxidative stress and inflammation and protects against multiple organ injury. However, the specific mechanisms responsible for protection against alcoholic injury remain not fully understood. In this study, we aim to investigate the effect and the regulatory mechanisms of naringin in the liver and whole body after alcohol exposure under zebrafish larvae system. MAIN METHODS: At 96 h post fertilization (hpf), larvae from wild-type (WT) and transgenic zebrafish, with liver-specific eGFP expression (Tg(lfabp10α:eGFP)), were exposed to 2% ethanol for 32 h to establish an ALD model. Different endpoints, such as morphological changes in liver shape and size, histological changes, oxidative stress-related free radical levels, apoptosis and the expression of certain genes, were chosen to verify the essential impact of naringin in alcohol-induced liver lesions. KEY FINDINGS: Subsequent experiments, including Oil red O, Nile red, pathological hematoxylin and eosin (H&E), and TUNEL staining and qPCR, revealed that naringin treatment reduced alcoholic hepatic steatosis, and this inhibitory effect was dose dependent. Specifically, a 25 mg/L dose resulted in an almost normal response. SIGNIFICANCE: This finding suggested that naringin may inhibit alcoholic-induced liver steatosis and injury by attenuating lipid accumulation and reducing oxidative stress and apoptosis.


Assuntos
Fígado Gorduroso Alcoólico/prevenção & controle , Flavanonas/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Hepatopatias Alcoólicas/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos , Animais , Animais Geneticamente Modificados , Apoptose/efeitos dos fármacos , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Etanol/efeitos adversos , Flavanonas/administração & dosagem , Proteínas de Fluorescência Verde/genética , Marcação In Situ das Extremidades Cortadas , Larva , Reação em Cadeia da Polimerase em Tempo Real , Peixe-Zebra
13.
J Nat Med ; 73(1): 179-189, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30377904

RESUMO

The present study was designed to investigate the effects of betulinic acid on human hepatic stellate cells in vitro and C57BL/6 mice in vivo, as well as the signaling pathways involved. In this study, we explored the effects of betulinic acid on expression of alpha smooth muscle actin and autophagy-related proteins. Betulinic acid reduced pathological damage associated with liver fibrosis, as well as serum platelet-derived growth factor and serum hydroxyproline levels. Furthermore, betulinic acid downregulated the expression of alpha smooth muscle actin and type I collagen in mouse liver and upregulated the expression of microtubule-associated protein light chain 3B and autophagy-related gene 7 at the gene and protein levels. LC3II expression was increased and alpha smooth muscle actin expression was decreased in betulinic acid-treated hepatic stellate cells. Interventions with bafilomycin A1 and mCherry-GFP-LC3 adenoviruses promoted the formation of autophagosomes in hepatic stellate cells and the development of autophagic flow. Our study found that mitogen-activated protein kinase/extracellular signal-regulated kinase may be involved in the effects of betulinic acid on liver fibrosis. The present study suggests that betulinic acid has anti-hepatic fibrosis activity by inducing autophagy and could serve as a promising new agent for treating hepatic fibrosis.


Assuntos
Cirrose Hepática/tratamento farmacológico , Triterpenos/uso terapêutico , Animais , Autofagia , MAP Quinases Reguladas por Sinal Extracelular/efeitos dos fármacos , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Humanos , Cirrose Hepática/patologia , Camundongos Endogâmicos C57BL , Triterpenos Pentacíclicos , Triterpenos/farmacologia
14.
J Pharmacol Sci ; 138(1): 46-53, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-30245287

RESUMO

Hepatic steatosis is the early stage of alcoholic liver disease (ALD), may progress to steatohepatitis, fibrosis even cirrhosis. Polydatin, the primary active component of Polygonum cuspidatum Sieb. et Zucc, has been recognized to possess hepatoprotective and anti-inflammatory properties. To investigate whether polydatin alleviates ethanol induced liver injury and to elucidate the underlying molecular mechanisms, zebrafish larvae at 4 days post-fertilization (dpf) were exposed to 350 mmol/L of ethanol for 32 h, then treated with polydatin for 48 h. Oil red O, Nile Red and H&E staining were used to analyze the pathological changes in liver. The mRNA levels were measured by quantitative PCR and the antioxidant capacity was detected using H2O2-specific fluorescent probe. Here, polydatin strongly alleviated hepatic steatosis and decreased the expression levels of alcohol and lipid metabolism-related genes, including CYP2Y3, CYP3A65, HMGCRa, HMGCRb and FASN. Additionally, polydatin inhibited oxidative stress in the liver according to fluorescent probe. Moreover, significantly up-regulated expression of DNA damage-related genes (CHOP, GADD45αa) revealed that polydatin attenuated hepatic apoptosis in larvae. In conclusion, polydatin may improve the liver function of zebrafish with acute alcoholic liver injury through attenuating hepatic fat accumulation, ameliorating lipid and ethanol metabolism and reducing oxidative stress and DNA damage.


Assuntos
Anti-Inflamatórios , Antioxidantes , Glucosídeos/farmacologia , Metabolismo dos Lipídeos/efeitos dos fármacos , Hepatopatias Alcoólicas/tratamento farmacológico , Hepatopatias Alcoólicas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Fitoterapia , Estilbenos/farmacologia , Peixe-Zebra , Animais , Hidrocarboneto de Aril Hidroxilases/genética , Hidrocarboneto de Aril Hidroxilases/metabolismo , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Família 3 do Citocromo P450/genética , Família 3 do Citocromo P450/metabolismo , Dano ao DNA/genética , Fallopia japonica/química , Expressão Gênica/efeitos dos fármacos , Glucosídeos/isolamento & purificação , Glucosídeos/uso terapêutico , Metabolismo dos Lipídeos/genética , Hepatopatias Alcoólicas/genética , Hepatopatias Alcoólicas/patologia , Proteínas Nucleares/genética , Proteínas Nucleares/metabolismo , Oxirredutases N-Desmetilantes/genética , Oxirredutases N-Desmetilantes/metabolismo , Estilbenos/isolamento & purificação , Estilbenos/uso terapêutico , Proteínas de Peixe-Zebra/genética , Proteínas de Peixe-Zebra/metabolismo
15.
J Nanosci Nanotechnol ; 13(11): 7386-90, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24245260

RESUMO

Carbon nanotube (CNT) has excellent electrical and thermal conductivity and high aspect ratio for X-ray tube cathode. However, CNT field emission cathode has been shown unstable field emission and short life time due to field evaporation by high current density and detachment by electrostatic force. An alternative approach in this direction is the introduction of CNT yarn, which is a one dimensional assembly of individual carbon nanotubes bonded by the Van der Waals force. Because CNT yarn is composed with many CNTs, CNT yarns are expected to increase current density and life time for X-ray tube applications. In this research, CNT yarn was fabricated by spinning of a super-aligned CNT forest and was characterized for application to an X-ray tube cathode. CNT yarn showed a high field emission current density and a long lifetime of over 450 hours. Applying the CNT yarn field emitter to the X-ray tube cathode, it was possible to obtain micro-scale resolution images. The relationship between the field emission properties and the microstructure evolution was investigated and the unraveling effect of the CNT yarn was discussed.


Assuntos
Eletrodos , Microeletrodos , Nanotubos de Carbono/química , Nanotubos de Carbono/ultraestrutura , Intensificação de Imagem Radiográfica/instrumentação , Radiografia/instrumentação , Condutividade Elétrica , Desenho de Equipamento , Análise de Falha de Equipamento , Teste de Materiais , Espalhamento de Radiação , Têxteis , Raios X
16.
J Nanosci Nanotechnol ; 13(11): 7669-74, 2013 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24245312

RESUMO

Since carbon nanotube (CNT) was first discovered in 1991, it has been considered as a viable type of conductive filler for electromagnetic wave absorption materials in the GHz range. In this paper, pearl-necklace-structure CNT/Ni nano-powders were fabricated by a polyol process as conductive fillers. Compared to synthesized CNT, pearl-necklace Ni-decorated CNT increased the electrical conductivity by an order of 1 due to the enhancement of the Ni-conductive network. Moreover, the decorated Ni particles prevented the agglomeration of CNTs by counterbalancing the Van der Walls interaction between the CNTs. A CNT/Ni nanocomposite showed a homogeneous dispersion in an epoxy-based matrix. This enhanced physical morphology and electrical properties lead to an increase in the loss tangent and reflection loss in the CNT/Ni/Epoxy nanocomposite compared to these characteristics of a CNT/Epoxy nanocomposite in range of 8-12 GHz. The electromagnetic wave absorption properties of CNT/Ni/epoxy nanocomposites will provide enormous opportunities for electronic applications where lightweight EMI shielding or electro-magnetic wave absorption properties are necessary.


Assuntos
Resinas Epóxi/química , Nanotubos de Carbono/química , Níquel/química , Absorção , Campos Eletromagnéticos , Resinas Epóxi/efeitos da radiação , Teste de Materiais , Nanotubos de Carbono/efeitos da radiação , Nanotubos de Carbono/ultraestrutura , Níquel/efeitos da radiação , Tamanho da Partícula , Espalhamento de Radiação
17.
J Nanosci Nanotechnol ; 11(7): 6076-9, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-22121661

RESUMO

Carbon nanotube has good electrical properties and a high aspect ratio, which enable it to obtain a high current at a low voltage due to its high field. Due to the life and uniformity of their emission tips, carbon nanotube field emitters are hard to commercialize. A field emitter with a three-dimensional (3D) structure was fabricated in this study to overcome such problems. In the 3D-structured field emitter, the field emission tips are located only at the vertical plane, where an enlarged field emission area can be attained. To fabricate the tip of the 3D-structured field emitter, carbon nanotube/silver nanocomposite powders were fabricated via molecular-level mixing and were sprayed at a substrate with good attachment and homogeneous dispersion between the CNT tips and the silver. The field emission properties of the 3D-structured field emitter were then determined and compared with those of a flat field emitter. The field emission area of the 3D-structured field emitter was found to be 4.5 times larger than that of the flat field emitter, with six times higher current density. Moreover, the 3D-structured field emitter had better stability than the flat field emitter. At a high gate field, the emission images of the 3D-structured field emitter showed light spots expanded towards the gate direction.

18.
J Nanosci Nanotechnol ; 10(1): 78-84, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20352814

RESUMO

A molecular-level mixing and controlled oxidation process is proposed as a novel fabrication technique for the production of CNT/Cu nanocomposite powders. The fabricated CNT/Cu2O nanocomposite powders showed microstructures with homogeneous dispersion of implanted CNTs in a Cu2O matrix. The CNT/Cu2O nanocomposite powders were reduced to CNT/Cu nanocomposite powders with H2 gas and then the as-prepared CNT/Cu nanocomposite powders were spark plasma sintered to fabricate CNT/Cu nanocomposites. The mechanical properties of the Cu and the CNT/Cu nanocomposites were characterized by tensile testing before and after hot compression. Before hot compression, the CNT/Cu nanocomposites were brittle, but after hot compression both yield strength and elongation were increased, while the yield strength of the Cu was decreased after hot compression. Hot compression enhanced the ductility and strength of the CNT/Cu nanocomposites due to alignment of Cu grains and CNTs. Electrical conductivity was also enhanced due to a reduced scattering of electrons because of the alignment of the CNTs and Cu grains as well as the annealing effects of the Cu matrix.


Assuntos
Cobre/química , Nanopartículas Metálicas/química , Nanocompostos/química , Nanotubos de Carbono/química , Condutividade Elétrica , Mecânica , Microscopia Eletrônica de Varredura , Microscopia Eletrônica de Transmissão , Oxirredução , Pós/química , Resistência à Tração
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