Combined Effects of Tauroursodeoxycholic Acid and Glutamine on Bacterial Translocation in Obstructive Jaundiced Rats:

Hatipoğlu, Ahmet; Oguz, Serhat; Gürcan, Şaban; Yalta, Tülin; Albayrak, Doğan; Erenoglu, Cengiz; Sagiroglu, Tamer; Sezer, Yavuz Atakan

doi:10.5152/balkanmedj.2013.7785

Cited by 4 publications

(2 citation statements)

References 35 publications

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“…They concluded that TUDCA therapy is safe and appears to be more effective than UDCA in improving biochemical parameters [ 40 ]. Our study evaluated the effect of TUDCA in a long term cholestasis mouse model, whereas other studies often study the effect during early cholestasis [ 41 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis

Paridaens

Raevens

Devisscher

et al. 2017

IJMS

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The role of endoplasmic reticulum stress and the unfolded protein response (UPR) in cholestatic liver disease and fibrosis is not fully unraveled. Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, has been shown to reduce endoplasmic reticulum (ER) stress and counteract apoptosis in different pathologies. We aimed to investigate the therapeutic potential of TUDCA in experimental secondary biliary liver fibrosis in mice, induced by common bile duct ligation. The kinetics of the hepatic UPR and apoptosis during the development of biliary fibrosis was studied by measuring markers at six different timepoints post-surgery by qPCR and Western blot. Next, we investigated the therapeutic potential of TUDCA, 10 mg/kg/day in drinking water, on liver damage (AST/ALT levels) and fibrosis (Sirius red-staining), in both a preventive and therapeutic setting. Common bile duct ligation resulted in the increased protein expression of CCAAT/enhancer-binding protein homologous protein (CHOP) at all timepoints, along with upregulation of pro-apoptotic caspase 3 and 12, tumor necrosis factor receptor superfamily, member 1A (TNFRsf1a) and Fas-Associated protein with Death Domain (FADD) expression. Treatment with TUDCA led to a significant reduction of liver fibrosis, accompanied by a slight reduction of liver damage, decreased hepatic protein expression of CHOP and reduced gene and protein expression of pro-apoptotic markers. These data indicate that TUDCA exerts a beneficial effect on liver fibrosis in a model of cholestatic liver disease, and suggest that this effect might, at least in part, be attributed to decreased hepatic UPR signaling and apoptotic cell death.

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Section: Discussionmentioning

confidence: 99%

Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis

Paridaens

Raevens

Devisscher

et al. 2017

IJMS

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“…Many clinical observations and experimental studies point to the frequent occurrence of different organ complications in patients with OJ. 19 The oxidative stress known to occur as a systemic response to cholestasis could give rise to the involvement of organs other than liver, such as the lung. 3 , 20 …”

Section: Discussionmentioning

confidence: 99%

L-carnitine reduces acute lung injury in experimental biliary obstruction

Kaya

Koca

Barut

et al. 2015

SMJ

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Objectives:To investigate the protective effects of L-carnitine (LC) on lungs in an experimental obstructive jaundice (OJ) model.Methods:This was conducted for 2 months between May 2011 and July 2011 at Suleyman Demirel University School of Medicine Experimental and Clinical Research Center, Isparta, Turkey. Thirty-eight Wistar-Albino rats with an average weight of 250-300 g were divided into 3 groups of control, OJ, and OJ + L-carnitine treatment (LCT). L-carnitine was injected intravenously into the tail vein at a dose of 50 mg/kg/day for 10 days to the LCT group. Animals were sacrificed 10 days later. Enzyme levels were measured in the lung tissue; malondialdehyde, myeloperoxidase (MPO), glutathione peroxidase (GSH-Px), catalase, and superoxide dismutase. Tumor necrosis factor-alfa, interleukin 6 (IL-6), IL-8, and C-reactive protein levels were studied in plasma samples. Histopathological changes in the lungs were examined.Results:There was a decreased in GSH-Px, MPO, and IL-8 levels (p<0.05) in the LCT group. The histopathological examination showed that neutrophil leukocyte infiltration and edema formation decreased and destruction of lung parenchyma disappeared following the treatment with LC (p<0.05).Conclusion:L-carnitine has a protective effect against lung damage due to experimental obstructive jaundice, possibly by altering anticytokine and antioxidant activity, and by decreasing the neutrophil migration.

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Dipeptiven® is safe in a rat model of moderate liver dysfunction

Bothe

Abele

Topp

et al. 2018

Clinical Nutrition Experimental

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s u m m a r yBackground & aims: Administration of glutamine in patients with liver failure is thought to possibly increase blood ammonia levels, thereby contributing to hepatic encephalopathy. In a rat model of moderate liver dysfunction with elevated plasma glutamine concentrations dose-dependent effects of intravenous alanylglutamine infusion on possible biochemical and histological signs of toxicity were investigated. Methods: Rats with moderate liver dysfunction resulting from alpha-naphthylisothiocyanate (ANIT) induced cholestasis received a 9 days continuous intravenous infusion of 0.5 g/kg/day or 3.0 g/ kg/day alanyl-glutamine (Dipeptiven ® ). Dose-dependent effects on liver injury were assessed by analyzing blood levels of ammonia, urea, ALT, AST, and ALP, glutamine, and histopathology. Results: Continuous intravenous infusion of 3.0 g/kg/day alanylglutamine increased plasma glutamine concentrations up to 30% without increasing blood ammonia levels or inducing astrocyte swelling. Alanyl-glutamine did not aggravate underlying liver injury shown by absent increase in plasma levels of ALT, AST, ALP and no signs of histopathologic alterations. Conclusions: Continuous intravenous infusion of alanyl-glutamine at 0.5 and 3.0 g/kg/day up to 9 consecutive days is safe in a rat model of moderate liver dysfunction based on ANIT-induced cholestasis.

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Combined Effects of Tauroursodeoxycholic Acid and Glutamine on Bacterial Translocation in Obstructive Jaundiced Rats:

Cited by 4 publications

References 35 publications

Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis

Modulation of the Unfolded Protein Response by Tauroursodeoxycholic Acid Counteracts Apoptotic Cell Death and Fibrosis in a Mouse Model for Secondary Biliary Liver Fibrosis

L-carnitine reduces acute lung injury in experimental biliary obstruction

Dipeptiven® is safe in a rat model of moderate liver dysfunction

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