NLRP3 inflammasome inhibition decreases -induced granulomatous inflammation and fibrosis in BALB/c mice.

To research the role of the NLRP3 inflammasome in -induced granuloma formation and liver fibrosis. In tests, BALB/c mice were used. shNLRP3 plasmid based on adeno-associated virus serotype 8 (AAV8-shNLRP3) was injected to block NLRP3 inflammasome via tail vein.

Effect of hepatocyte damage in hepatic fibrogenesis of patients infected with .

Schistosomiasis is a serious public health problem, and previous studies found that liver function and hepatic cells are damaged. To evaluate the serum parameters of liver function and fibrosis in schistosomiasis patients infected with (.) and analyze the correlations between liver function and serum fibrosis markers in patients infected with .

NLRP3 inflammasome activation results in liver inflammation and fibrosis in mice infected with Schistosoma japonicum in a Syk-dependent manner.

Granulomatous and fibrosing inflammation in response to soluble egg antigen (SEA) from Schistosoma japonicum (S. japonicum) is the main pathological process of S. japonicum infection.

MiR-375 and Doxorubicin Co-delivered by Liposomes for Combination Therapy of Hepatocellular Carcinoma.

Doxorubicin (DOX) is one of the most frequently used anti-cancer drugs and the front line option for hepatocellular carcinoma (HCC) treatment. However, the clinical applications of DOX are restricted largely due to its toxicity and chemoresistance. Here, we report that miR-375 and DOX were co-delivered by liposomes (named L-miR-375/DOX-NPs) for combination therapy of HCC and drug resistance reversion of DOX.

Activation of NLRP3 inflammasomes in mouse hepatic stellate cells during Schistosoma J. infection.

The major pathological changes during Schistosoma J. infection are characterized by granulomatous inflammation in the liver, a cellular immune response to schistosomal egg antigens. The molecular mechanisms initiating or promoting this schistosomal granulomatous inflammation remain poorly understood.

Endocannabinoids signaling: Molecular mechanisms of liver regulation and diseases.

The endocannabinoid system (ECS) includes endocannabinoids (eCBs), cannabinoid (CB) receptors and the enzymes that are responsible for endocannabinoid production and metabolism. The ECS has been reported to be present in both brain and peripheral tissues. Recent studies have indicated that eCBs and their receptors are involved in the development of various liver diseases.

Efficacy of telbivudine in the treatment of chronic hepatitis b and liver cirrhosis and its effect on immunological responses.

This study was aimed to evaluate the long-term effects of telbivudine (LdT) in the treatment of chronic hepatitis B (CHB) and HBV-related liver cirrhosis (LC) and to observe the changes of immunological responses during LdT treatment. Clinical data of 80 CHB and 28 HBV-related LC patients who were administered with LdT for 108 weeks and followed up were retrospectively analyzed. The liver function indicators including ALT, AST and γ-GT, HBV DNA copy number in serum and the rates of hepatitis B e antigen (HBeAg) seroconversion were analyzed before and 12, 24, 36, 48, 60, 72, 84, 96 and 108 weeks after LdT treatment in CHB and LC groups.

Upregulation of cannabinoid receptor-1 and fibrotic activation of mouse hepatic stellate cells during Schistosoma J. infection: role of NADPH oxidase.

The endocannabinoid system (CS) has been implicated in the development of hepatic fibrosis such as schistosomiasis-associated liver fibrosis (SSLF). However, the mechanisms mediating the action of the CS in hepatic fibrosis are unclear. The present study hypothesized that Schistosoma J.

[Expression of ASMase in alcoholic liver fibrosis in rats].

Objective: To investigate the expression of the lysosomal enzyme acid sphingomyelinase (ASMase) in alcohol-induced hepatic fibrosis using a rat model.

Methods: The model of liver fibrosis was induced by administration of alcohol and high fat diet using 20 rats. Six rats given no alcohol and normal diet served as the control group.

[Effects of anandamide on proliferation of and pErk expression in primary hepatic stellate cells of schistosome-induced liver fibrosis mice].

Objective: To investigate the potential therapeutic properties of the endogenous cannabinoid N-arachidonic acid aminoethanols (anandamide, AEA) in liver fibrosis by observing its affects on proliferation of and expression of phosphorylated-Erk (pErk) in primary hepatic stellate cells (HSCs) from a mouse model of schistosome-induced liver fibrosis.

Methods: The schistosome-induced liver fibrosis model was established by attaching cercaria to the skin on the ventral side of the mouse and allowing infection to occur via direct penetration. Six weeks later, the model was confirmed by pathological analysis of liver, with Masson trichrome staining showing collagen fiber deposition around the blood vessels and hematoxylin-eosin staining showing eosinophilic granuloma formation.

Schistosoma japonicum egg antigen up-regulates fibrogenesis and inhibits proliferation in primary hepatic stellate cells in a concentration-dependent manner.

Aim: To investigate the effects of different concentrations of Schistosoma japonicum (S. japonicum) egg antigen on fibrogenesis and apoptosis in primary hepatic stellate cells (HSCs).

Methods: A mouse model of schistosomiasis-associated liver fibrosis (SSLF) was established by infecting mice with schistosomal cercaria via the abdomen.

[Membrane cholesterol mediates the endocannabinoids-anandamide affection on HepG2 cells].

Objective: To study the effect of anandamide (AEA) on necrosis in HepG2 cells and to explore the role of AEA in progression of liver cancer.

Methods: Localization of the fatty acid hydrolytic enzyme (FAAH), cannabinoid receptors 1(CB1) and cannabinoid receptors 2 (CB2) proteins was detected in L02 and HepG2 cells using immunofluorescence. L02 and HepG2 cells were treated with different concentrations of AEA and methyl-beta-cyclodextrin, and the rates of cells necrosis were examined by PI stain.

Hepatic stellate cell-specific gene silencing induced by an artificial microRNA for antifibrosis in vitro.

Background: We previously reported that the anti-transforming growth factor-beta1 (TGF-beta1) ribozymes directed by T7 and CMV promoters could reverse the character of activated hepatic stellate cells (HSCs) in vitro and improve fibrotic pathology in vivo. However, nonspecific elimination of the effects of TGF-beta1 without selectivity might have unfavorable consequences, such as overwhelming inflammation, tissue necrosis, etc.

Aims: To establish an activated-HSC-specific gene silencing method and validate its feasibility for antifibrosis in vitro.

Endocannabinoids anandamide and its cannabinoid receptors in liver fibrosis after murine schistosomiasis.

This study examined endogenous cannabinoid (ECB)-anandamide (AEA) and its cannabinoid receptors (CBR) in mice liver with the development of schistosoma japonicum. Mice were infected with schistosoma by means of pasting the cercaria onto their abdomens. Liver fibrosis was pathologically confirmed nine weeks after the infection.

[Effects of norepinephrine on the proliferation and activation of rat hepatic stellate cells].

Objective: To elucidate the relationship between rat hepatic stellate cells (HSC) and sympathetic neurotransmitter norepinephrine (NE) during liver fibrosis.

Methods: Using immunofluorescence and RT-PCR, the expressions of a1 and b2-adrenoceptors in activated HSC were detected. Methyl thiazolyl tetrazolium (MTT) was adopted to investigate the effect of NE on the proliferation of HSC.

[Effects of anandamide on the activation and proliferation of hepatic stellate cells through cannabinoid-2 receptors].

Objective: To study the effects of endogenous cannabinoid anandamide (AEA) and its putative endocannabinoid receptors (CBR) on the activation and proliferation of hepatic stellate cells (HSC) and to study the role played by AEA during liver fibrosis.

Methods: By using immunofluorescence and cell culture, the expression of CBR 1 and 2 in the PDGF-stimulated HSCs was investigated. By using PCR and Western-blot, the effects of 10, 20mumol/L AEA and CBR2 antagonist AM630 on the cultured and activated HSC were observed.

[The effects of sympathetic neurotransmitters and adrenergic receptors on liver fibrosis in murine schistosomiasis].

Objective: To investigate the effects of sympathetic neurotransmitters and adrenergic receptors on liver fibrosis in murine schistosomiasis.

Methods: Mice were infestated with schistosoma by means of pasting cercariae on their abdomens. Thirty mice were randomly divided into a control group and a model group.

Low-dose ATRA supplementation abolishes PRM formation in rat liver and ameliorates ethanol-induced liver injury.

The effects of all-trans-retinoic acid (ATRA) in low doses supplementation on concentrations of polar retinoid metabolites (PRM) and retinoids in the ethanol-fed rat liver, and on hepatocyte injury were investigated. The rat model of alcoholic liver disease (ALD) was induced by intragastric infusion of ethanol, and then the rats were administrated with ATRA in two different doses (150 microg/kg body weight and 1.5 mg/kg body weight) for 4 weeks.

[Expression and significance of hypoxia inducible factor-1 alpha in hepatocellular carcinoma tissues].

Objectives: To investigate the expression and significance of HIF1 alpha in hepatocellular carcinoma (HCC) tissues and in hepatoma carcinoma cell line HepG2.

Methods: The expression of the HIF1 alpha mRNA and protein were detected with immunohistochemistry (IHC), Western blot and RT-PCR techniques in HCC, normal liver tissues and HepG2. Their relationship with the pathological characteristics of the HCC was also analyzed.

Correlation between pulmonary endothelin receptors and alveolar-arterial oxygen gradient in rats with hepatopulmonary syndrome.

The correlation between pulmonary endothelin receptors and alveolar-arterial oxygen gradient (A-aDO2) in rats with hepatopulmonary syndrome was investigated. Animals were divided into 2 groups: Sham-operated (Sham) group and common bile duct ligation (CBDL) group. Arterial blood gas was evaluated by a blood gas analyzer.

[The relationship between the plasma homocysteine level and the polymorphism of MTHFR gene C667T in liver cirrhosis].

Objective: To study the relationship between the plasma homocysteine (HCY) level and the polymorphism of N(5), N(10)-methylenetetrahydrofolate reductase (MTHFR) gene C667T in liver cirrhosis.

Methods: 112 normal subjects and 87 liver cirrhosis patients were recruited in the study. Their plasma HCY levels were measured using high performance liquid chromatography with fluorescence detection and polymorphisms of their MTHFR gene were analyzed using PCR-RFLP.

The docosatriene protectin D1 is produced by TH2 skewing and promotes human T cell apoptosis via lipid raft clustering.

Docosahexaenoic acid, a major omega-3 fatty acid in human brain, synapses, retina, and other neural tissues, displays beneficial actions in neuronal development, cancer, and inflammatory diseases by mechanisms that remain to be elucidated. In this study we found, using lipid mediator informatics employing liquid chromatography-tandem mass spectrometry, that (10,17S)-docosatriene/neuroprotectin D1, now termed protectin D1 (PD1), is generated from docosahexaenoic acid by T helper type 2-skewed peripheral blood mononuclear cells in a lipoxygenase-dependent manner. PD1 blocked T cell migration in vivo, inhibited tumor necrosis factor alpha and interferon-gamma secretion, and promoted apoptosis mediated by raft clustering.

[Clinical study of lamivudine and interferon combinate administration to inhibit hepatitis B virus replication].

Objective: To explore a new strategy for effective and economical anti-virus therapy for HBV infection, we conducted a sequence administration of lamivudine and interferon alpha 1b to evaluate its effects on HBV replication and rebound as well as YMDD mutation induced by lamivudine.

Methods: 150 HBV patients having at least 6 months history of infection were assigned randomly into 5 groups. Each group of these patients was either treated with lamivudine, interferon alpha 1b, lamivudine combined with interferon, sequence administration of lamivudine and interferon (sequence group) or no anti-virus therapy (control group) for 12 months.

Experimental study of effect of Ganyanping on fibrosis in rat livers.

Aim: To observe the effects of Ganyanping on CCl(4)-induced hepatic fibrosis in rats.

Methods: The rats were separated randomly into five groups. Groups A to group D, each consisting of 15 rats, were for different tests, while 8 rats were used as normal controls (N).