The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform

E Roeb - One of the best experts on this subject based on the ideXlab platform.

H.m. Dashti - One of the best experts on this subject based on the ideXlab platform.

  • Cholangiocarcinoma and liver cirrhosis in relation to changes due to Thioacetamide
    Molecular and Cellular Biochemistry, 2000
    Co-Authors: A. Al-bader, T.c. Mathew, H. Abul, H. Al-sayer, P.k. Singal, H.m. Dashti
    Abstract:

    Different doses of Thioacetamide (0.05, 0.1 and 0.15%) were used to induce liver cirrhosis in Wistar rats. Thioacetamide at 0.5% caused cirrhosis by the twelfth week of treatment. A severe bile duct proliferation and cholangiocarcinoma was seen at longer intervals. Animals treated with higher doses (0.1 and 0.15%) of Thioacetamide developed more severe intense degenerative changes in the liver and died in the twelfth and eighth week respectively. The serum and tissue contents of Zn and Cu changed in a characteristic fashion that was consistent with the severity of the liver damage. Serum Zn and Cu concentrations were at their lowest in the animals that developed severe degenerative liver and died at higher dose (0.15%) of Thioacetamide. This study indicates that treatment of rats with 0.05% thiocetamide is more effective and appropriate for the induction of liver cirrhosis. Continued administration of the drug at this dosage led to the development of further changes in the liver. This model may be suitable for studying these long term changes that occur in the liver and lead to cirrhosis. Events that precede the development of severe bile duct proliferation and cholangiocarcinoma may also be studied.

  • Selenium and Liver Cirrhosis
    Molecular and Cellular Biochemistry, 1998
    Co-Authors: A. Al-bader, T.c. Mathew, H. Abul, T. Hussain, M. Al-moosawi, H.m. Dashti
    Abstract:

    Effects of selenium deficiency, induced by Thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by Thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the Thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by Thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.

Elliot M Berry - One of the best experts on this subject based on the ideXlab platform.

  • cannabidiol improves brain and liver function in a fulminant hepatic failure induced model of hepatic encephalopathy in mice
    British Journal of Pharmacology, 2011
    Co-Authors: Yosefa Avraham, Nikolaos Grigoriadis, Theofilos Poutahidis, L Vorobiev, Iddo Magen, Yaron Ilan, Raphael Mechoulam, Elliot M Berry
    Abstract:

    BACKGROUND AND PURPOSE: Hepatic encephalopathy is a neuropsychiatric disorder of complex pathogenesis caused by acute or chronic liver failure. We investigated the effects of cannabidiol, a non-psychoactive constituent of Cannabis sativa with anti-inflammatory properties that activates the 5-hydroxytryptamine receptor 5-HT(1A) , on brain and liver functions in a model of hepatic encephalopathy associated with fulminant hepatic failure induced in mice by Thioacetamide. EXPERIMENTAL APPROACH: Female Sabra mice were injected with either saline or Thioacetamide and were treated with either vehicle or cannabidiol. Neurological and motor functions were evaluated 2 and 3 days, respectively, after induction of hepatic failure, after which brains and livers were removed for histopathological analysis and blood was drawn for analysis of plasma liver enzymes. In a separate group of animals, cognitive function was tested after 8 days and brain 5-HT levels were measured 12 days after induction of hepatic failure. KEY RESULTS: Neurological and cognitive functions were severely impaired in Thioacetamide-treated mice and were restored by cannabidiol. Similarly, decreased motor activity in Thioacetamide-treated mice was partially restored by cannabidiol. Increased plasma levels of ammonia, bilirubin and liver enzymes, as well as enhanced 5-HT levels in Thioacetamide-treated mice were normalized following cannabidiol administration. Likewise, astrogliosis in the brains of Thioacetamide-treated mice was moderated after cannabidiol treatment. CONCLUSIONS AND IMPLICATIONS: Cannabidiol restores liver function, normalizes 5-HT levels and improves brain pathology in accordance with normalization of brain function. Therefore, the effects of cannabidiol may result from a combination of its actions in the liver and brain.

  • cannabinoids and capsaicin improve liver function following Thioacetamide induced acute injury in mice
    The American Journal of Gastroenterology, 2008
    Co-Authors: Yosefa Avraham, Nikolaos Grigoriadis, Iddo Magen, Yaron Ilan, Raphael Mechoulam, Olga Zolotarev, Theofilos Pautahidis, Lia Vorobiav, Andreas Zimmer, Elliot M Berry
    Abstract:

    OBJECTIVES: We have shown the beneficial effects of cannabinoids in a murine model of hepatic encephalopathy following Thioacetamide and now report their effects on the liver injury. METHODS: Fulminant hepatic failure (FHF) was induced by administration of 200 mg/kg Thioacetamide to wild-type (WT) and CB2 Knockout (KO) mice. Twenty-four hours later, mice were injected with 2-arachidonoylglycerol (CB1, CB2, and TRPV1 agonist), HU308 (CB2 agonist), SR141716 A (CB1 receptor blocker), SR141716 A+2-AG, and SR144528 (CB2 receptor blocker), capsaicin and capsazepine (TRPV1 agonist and antagonist receptors). Mice were sacrificed 2 days after Thioacetamide administration (day 3) and liver biochemistry and histopathology as well as evaluation of 2-arachidonoylglycerol levels were performed on liver tissue. RESULTS: Liver histopathology undertaken 48 h after Thioacetamide showed evidence of necrosis and inflammation. SR141716 A, HU308, and 2-arachidonoylglycerol reduced inflammation and promoted regeneration 1 day after their administration. Liver enzymes increased after Thioacetamide administration and were reversed after SR141716 A and 2-arachidonoylglycerol administered alone or combined, HU-308, but not SR144528. Thus, the beneficial effects mediated through CB2 receptors. However, CB2 KO mice still modulated liver function via the TRPV1 receptors. Capsaicin improved both liver pathology and function in WT Thioacetamide-treated mice, while capsazepine impaired it. CONCLUSIONS: The similar pattern found between the effect of cannabinoids and their antagonists on brain and liver indicated that the therapeutic effect might be directed by the improvement in both organs through CB2 receptors and/or TRPV1 receptors. Modulation of these systems may have therapeutic potential.

Junji Yodoi - One of the best experts on this subject based on the ideXlab platform.

  • overexpression of thioredoxin prevents Thioacetamide induced hepatic fibrosis in mice
    Journal of Hepatology, 2005
    Co-Authors: Hiroaki Okuyama, Hajime Nakamura, Yasuyuki Shimahara, Naoki Uyama, Yongwon Kwon, Norifumi Kawada, Yoshio Yamaoka, Junji Yodoi
    Abstract:

    Background/Aims Thioredoxin is a small redox-active protein with anti-oxidant and anti-apoptotic effects. We have previously reported that Thioacetamide-induced acute hepatitis was attenuated in thioredoxin transgenic mice. The aim of the present study was to investigate the protective effect of thioredoxin for hepatic fibrosis. Methods We subjected thioredoxin transgenic mice to Thioacetamide-induced hepatic fibrosis. We also studied the effect of thioredoxin on the activation process of primary-cultured hepatic stellate cell. Results The expression of endogenous thioredoxin was induced in hepatocytes of Thioacetamide-induced murine and rat fibrotic livers. Overexpression of thioredoxin inhibited tumor necrosis factor-α-induced apoptosis of HepG2 cells. Thioacetamide-induced fibrosis and accumulation of malondialdehyde were suppressed in transgenic mice as compared with wild type mice. Hepatic stellate cells isolated from transgenic mice were less proliferative than those isolated from wild type mice. Recombinant thioredoxin significantly inhibited DNA synthesis of primary-cultured stellate cells under serum or platelet-derived growth factor stimulation. Conclusions Thioredoxin has a potential to attenuate hepatic fibrosis via suppressing oxidative stress and inhibiting proliferation of stellate cells.

Rebeca Salguero Palacios - One of the best experts on this subject based on the ideXlab platform.