Sequential changes in redox status and nitric oxide synthases expression in the liver after bile duct ligation

Vázquez-Gil, M.José; Mesonero, M.José; Flores, Olga; Criado, M.; Hidalgo, F.; Arévalo, Miguel; Sánchez‐Rodríguez, Ángel; Tuñón, María J.; López‐Novoa, José M.; Esteller, A

doi:10.1016/j.lfs.2004.01.017

Cited by 23 publications

(27 citation statements)

References 54 publications

(59 reference statements)

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“…Bile duct ligation is an established method for investigating cholestasis and hepatic fibrosis, which leads to changes in the equilibrium between antioxidant and prooxidant activities [19]. The deposition of hydrophobic bile acids damages the mitochondrial electron transport chain and enhances the production of ROS.…”

Section: Discussionmentioning

confidence: 99%

Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

Tian

Zhao

Guo

et al. 2017

BioMed Research International

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Background. The sympathetic nervous system (SNS) is responsible for hepatic stellate cells (HSCs) activation and the accumulation of collagen that occurs in hepatic fibrogenesis. Carvedilol has been widely used for the complication of hepatic cirrhosis in the clinic. Furthermore, it has powerful antioxidant properties. We assessed the potential antifibrotic effects of carvedilol and the underlying mechanisms that may further enhance its clinical benefits. Methods. Using a bile duct ligation rat model of hepatic fibrosis, we studied the effects of carvedilol on the fibrosis, collagen deposition, and oxidative stress based on histology, immunohistochemistry, western blot, and RT-PCR analyses. Results. Carvedilol attenuated liver fibrosis, as evidenced by reduced hydroxyproline content and the accumulation of collagen, downregulated TIMP-1 and TIMP-2, and upregulated MMP-13. MMP-2 was an exception, which was decreased after carvedilol treatment for 2 weeks and upregulated after carvedilol treatment for 4 weeks. Carvedilol reduced the activation of HSCs, decreased the induction of collagen, transforming growth factor-β1, and MDA content, and strengthened the SOD activity. The antifibrotic effects were augmented as dosages increased. Conclusions. The study indicates that carvedilol attenuated hepatic fibrosis in a dose-dependent manner. It can decrease collagen accumulation and HSCs activation by the amelioration of oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

Tian

Zhao

Guo

et al. 2017

BioMed Research International

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show abstract

“…In this situation, it was not possible to discriminate between the role of NO-derived from the iNOS or the eNOS. These two enzymes can be differentially expressed in the liver, the iNOS in pathological whereas the eNOS in physiological situations, thus suggesting distinct roles in liver [18][19][20]37]. Therefore, to study the specific role of NO-derived from iNOS, we have used mice with a targeted disruption of the iNOS gene.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of inducible nitric oxide synthase protects against liver injury induced by mycobacterial infection and endotoxins

Guler

Olleros

Vesin

et al. 2004

Journal of Hepatology

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“…Liver tissue was homogenized as previously described [29][30][31] and proteins were separated by SDS-PAGE and transferred to PVDF membranes. Membranes were immunobloted with antibodies antiphospho-AMPK (Thr172) (1:1000) and anti-AMPK (1:1000) (Cell Signalling, Beverly, MA), anti-eNOS (1:500) and anti-i-iNOS (1:1000) (Transduction Laboratories, Lexington.…”

Section: Western Blot Analysis Of Ampk and Nosmentioning

confidence: 99%

Adenosine monophosphate-activated protein kinase and nitric oxide in rat steatotic liver transplantation

Carrasco-Chaumel

Roselló‐Catafau

Bartrons

et al. 2005

Journal of Hepatology

106

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Sequential changes in redox status and nitric oxide synthases expression in the liver after bile duct ligation

Cited by 23 publications

References 54 publications

Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

Carvedilol Attenuates the Progression of Hepatic Fibrosis Induced by Bile Duct Ligation

Inhibition of inducible nitric oxide synthase protects against liver injury induced by mycobacterial infection and endotoxins

Adenosine monophosphate-activated protein kinase and nitric oxide in rat steatotic liver transplantation

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