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#27891207   2016/11/28 Save this To Up

The Antiapoptosis Effect of Glycyrrhizate on HepG2 Cells Induced by Hydrogen Peroxide.

This study demonstrated that glycyrrhizate (GAS) could protect HEPG2 cells against damage and apoptosis induced by H2O2 (1600 μM, 4 h). Cell viability assay revealed that GAS was noncytotoxity at concentration 125 µg/mL, and GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) protected HepG2 cells against H2O2-induced cytotoxicity. H2O2 induced the HepG2 cells apoptosis, obvious morphologic changes were observed after Hochest 33258 staining, and more apoptotic cells were counted in flow cytometry assay compared to that of the natural group. Pretreatment GAS (5 μg/mL, 25 μg/mL, and 125 μg/mL) prior to H2O2 reverses the morphologic changes and reduced the apoptotic cells in HepG2 cells. GAS reduced the release of MDA, increased the activities of superoxide dismutase, and diminished the release of ALT and AST during oxidative stress in HepG2 cells. After Elisa kit detecting, GAS inhibited the caspase activity induced by H2O2, GAS decreased the level of caspase-3 and caspase-9 from mitochondria in dose-dependent manner. Western blot results showed that pretreatment GAS upregulated the expression of Bcl-2 and decreased the expression of Bax. These results reveal that GAS has the cytoprotection in HepG2 cells during ROS exposure by inhibiting the caspase activity in the mitochondria and influencing apoptogenic factors of the expression of Bax and Bcl-2.

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#27667108   2016/09/26 Save this To Up

[Role of endoplasmic reticulum stress-mediated glycogen synthase kinase 3β activity in pathogenesis of acute liver failure in mice].

Objective: To study the role of endoplasmic reticulum (ER) stress-mediated glycogen synthase kinase 3β (GSK3β) activity in the pathological process of liver injury in acute liver failure (ALF) mice. Methods: ALF model was established by intraperitoneal injection of D-galactosamine/lipopolysaccharide (D-GalN/LPS) in C57BL/6 mice. The mice were divided into control group (n=10), ALF model group (n=18), 4-phenylbutyrate (4-PBA, an ER stress inhibitor) group (n=18) and SB216763 (a specific inhibitor of GSK3β) group (n=16). The serum alanine transaminase (ALT) and aspartate transaminase (AST) levels were measured to reflect the liver function, liver injury was assessed by observing pathological changes of liver tissue, the levels of proteins in liver tissue were analyzed by Western blotting, the activity of GSK3β in liver tissue was detected using GSK3β activity assay kit, and the survival rate of hepatocyte was measured by methyl thiazolyl tetrazolium (MTT) assay. Results: In in vivo experiment, the expression levels of ER stress markers, glucose-regulated protein 78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP), were upregulated during the progression of D-GalN/LPS-induced ALF, indicating activation of severe ER stress and increased activity of GSK3β. Compared with the model group, inhibition of ER stress by 4-PBA improved liver function[ALT: (365.4±58.6) U/L vs (1 094.5±201.5) U/L, P<0.05; AST: (555.1±60.8) U/L vs (1 444.3±533.7) U/L, P<0.05)and pathological injury, also decreased the activity of GSK3β (2.6±0.3 vs 4.6±1.3, P<0.05). Inhibition of GSK3β activity was shown to alleviate liver injury in ALF by reducing the expression levels of GRP78 and CHOP. The in vitro experiment of tunicamycin-induced hepatocyte apoptosis showed that inhibition of GSK3β activity increased the cell survival rate. Conclusion: In ALF induced by D-GalN/LPS, severe ER stress may accelerate the development and progress of ALF by upregulating the activity of GSK3β.

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#26690542   2015/12/22 Save this To Up

Ameliorative effects of β-sitosterol on some biochemical indices of hypertension in wistar albino rats.

Cardiovascular diseases presently rank high as leading causes of death globally. The increasing acceptability of phytomedicine is due to the increasing inefficacy of many modern drugs used for the control of many diseases. The aim of this study was to investigate the ameliorative effects of β-sitosterol (BSS) in comparison with lisinopril, a standard antihypertensive drug, on certain biochemical hypertensive parameters in rats.

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#23058009   2012/10/12 Save this To Up

Melatonin protection against burn-induced hepatic injury by down-regulation of nuclear factor kappa B activation.

Melatonin exhibits a wide variety of biological activity including antioxidant and anti-inflammatory effects. We have previously reported its protective effect on hepatic oxidative hepatic injury in burns. In this study, we investigated the role of nuclear factor kappa B (NF-κB) in melatonin-mediated protection against liver injury by using the burned-rat model. Melatonin (N-acetyl-5-methoxytriptamin, 10mg/kg (-1), i.p.) was administered immediately and 12 hours after thermal skin injury. Hepatic NF-κB expression was determined by Western blotting. TNF-α level in liver homogenate was quantified using enzyme-linked immunosorbent assay (ELISA) kit. Plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were determined to assess liver injury at the 24th hour after burns. Thermal skin injury caused significant elevation of hepatic NF-κB expression by 48 percent, TNF-α level by 55 percent and plasma AST and ALT activities by 2- and 3-fold, respectively, in comparison with normal control rats. Treatment with melatonin decreased significantly elevated hepatic NF-κB activity and TNF-α, maintaining the levels close to the control values Melatonin suppressed the elevation of plasma AST and ALT activities (p less than 0.001), which remained significantly increased compared to controls. In conclusion, thermal skin injury causes hepatic NF-κB activation that may mediate the release of hepatic TNF-α and contribute to liver damage. Melatonin protects against burn-induced hepatic injury as to a certain extent this effect may result from the suppression of NF-κB-mediated inflammatory response.

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#22641092   2012/09/18 Save this To Up

Nilotinib protects the murine liver from ischemia/reperfusion injury.

The mitogen-activated protein kinases (MAPKs), c-Jun N-terminal kinase (JNK), and p38, mediate liver ischemia/reperfusion (I/R) injury via cell death and inflammatory cytokine expression, respectively. Nilotinib is an orally available receptor tyrosine kinase inhibitor used for chronic myelogenous leukemia that also has in vitro activity against JNK and p38. In this study, we examine its therapeutic potential against hepatic I/R injury.

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#20975272   2010/11/22 Save this To Up

Assessment of clinical utility of low and high normal alanine aminotransferase values in patients with chronic hepatitis B virus infection in Bangladesh.

There is a lack of consensus about the currently accepted range of normal values for serum alanine aminotransferase (ALT) levels because some investigators have claimed that the true values are significantly lower than those listed by kit manufacturers.

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#20551524   2010/06/16 Save this To Up

Predictors of histological activity and fibrosis in chronic Hepatitis C infection: a study from North India.

The role of hepatitis C virus (HCV) genotypes in the severity of liver disease is still debatable and there is an occasional published report from India. The aim of this study is to assess the role of HCV genotypes in severity of liver disease in Indian patients. An attempt has also been made to perform a multivariate analysis to identify the predictors of severity of liver disease in chronic HCV infection.

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#19291919   2009/03/18 Save this To Up

Association of Ki67 with raised transaminases in hepatocellular carcinoma.

Transaminase enzymes, alanine (ALT) and aspartate transaminase (AST), have been reported to be raised and implicated to have prognostic value in hepatocellular carcinoma (HCC). Ki67, a marker of cellular proliferative activity, has also been noted to be increased in HCC. A study was conducted at the Department of Pathology, Faculty of Medicine, University of Malaya, Kuala Lumpur to determine the possible association of proliferative activity, as determined by Ki67, with the transaminase enzymes. 31 cases of histologically diagnosed HCC who underwent tumour resection were retrieved from departmental archives. The patients' ages ranged between 40 to 79 years with a mean of 58.3 years. There was a male preponderance with M:F = 2.9:1. Ethnic Chinese formed 83.9% of the cases. 4 microm sections, cut from the formalin-fixed, paraffin-embedded tumour tissue block of each case, were immunohistochemically stained with Ki67 (DAKO monoclonal MIB-1) using the commercial DakoCytomation EnVision+System-HRP kit. The latest ALT and AST levels, assayed within 7 days prior to tumour resection, were retrieved from the patients' case records. 24 (77.4%) HCC demonstrated elevation of either ALT and/or AST. 27 (87.1%) HCC were immunopositive for Ki67. Ki67 immunoexpression was significantly correlated with raised transaminases (p<0.05). Hypothetically, the mechanism by which this phenomenon may occur may simply be release of transaminases due to destruction of hepatocytes by the cancer. Thus rising levels of the transaminases could signal a more rapid growth of the tumour and these routinely performed tests can be of prognostic value in management of HCC patients.

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#16552805   2006/03/22 Save this To Up

In vitro and in vivo protective effects of proteoglycan isolated from mycelia of Ganoderma lucidum on carbon tetrachloride-induced liver injury.

To investigate the possible mechanism of the protective effects of a bioactive fraction,Ganoderma lucidum proteoglycan (GLPG) isolated from Ganoderma lucidum mycelia, against carbon tetrachloride-induced liver injury.

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#16437600   2006/01/26 Save this To Up

Nuclear factor-kappaB decoy oligodeoxynucleotides attenuates ischemia/reperfusion injury in rat liver graft.

To evaluate the protective effect of NF-kappaB decoy oligodeoxynucleotides (ODNs) on ischemia/reperfusion (I/R) injury in rat liver graft.

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