Chronic administration of aminoguanidine reduces vascular nitric oxide production and attenuates liver damage in bile duct‐ligated rats

Wei, Changli; Hon, Wei; Lee, Kang-Hoe; Khoo, Hoon‐Eng

doi:10.1111/j.1478-3231.2005.01063.x

Cited by 18 publications

(14 citation statements)

References 44 publications

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“…In VSMCs (vascular smooth muscle cells) and a mouse macrophage cell line, administration of UDCA was found to inhibit the activity of iNOS and the LPS-induced release of NO [24,38,39]. A previous study has shown that inhibition of hepatic iNOS expression can attenuate damage in livers of BDL rats [39]. In the present study, the inhibition of hepatic iNOS-related nitrite release was accompanied by the amelioration of hepatic inflammation in BDL-UDCA rats.…”

Section: Figure 6 Representative Histology Sections Of Livers From Bdsupporting

confidence: 55%

“…We have also shown in the present study that treatment of BDL rats for 1 month with UDCA significantly inhibited hepatic iNOS expression and the corresponding hepatic levels of nitrite. In VSMCs (vascular smooth muscle cells) and a mouse macrophage cell line, administration of UDCA was found to inhibit the activity of iNOS and the LPS-induced release of NO [24,38,39]. A previous study has shown that inhibition of hepatic iNOS expression can attenuate damage in livers of BDL rats [39].…”

Section: Figure 6 Representative Histology Sections Of Livers From Bdmentioning

confidence: 95%

“…Wei et al [39] have reported that chronic administration of a specific inhibitor of iNOS, aminoguanidine, decreased systemic NO levels, as well as suppressed iNOS expression and activity in aorta, and improved liver function in BDL rats [39]. A previous study has found that UDCA inhibits the release of iNOSrelated NO in aortic smooth muscle cells [24].…”

Section: Figure 6 Representative Histology Sections Of Livers From Bdmentioning

confidence: 96%

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Chronic administration of ursodeoxycholic acid decreases portal pressure in rats with biliary cirrhosis

Yang

Huang²,

Lee

et al. 2008

Clinical Science

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Liver cirrhosis is characterized by increased IHR (intrahepatic resistance) and lipid peroxidation, and decreased antioxidative defence. The present study investigates the effects of administration for 1 month of the antioxidant UDCA (ursodeoxycholic acid) in BDL (bile-duct-ligated) cirrhotic rats. Splanchnic haemodynamics, IHR, hepatic levels of TBARS (thiobarbituric acid-reacting substances), GSH (glutathione), SOD (superoxide dismutase) activity, nitrite, PIIINP (N-terminal propeptide of type III procollagen) and collagen deposition, histological examination of liver, mRNA expression of PIIIP-alpha1 (type III procollagen) and TGF-beta1 (transforming growth factor-beta1), protein expression of TXS (thromboxane synthase) and iNOS (inducible NO synthase), and TXA2 (thromboxane A2) production in liver perfusates were measured. The results showed that portal pressure and IHR, hepatic levels of PIIINP, hepatic collagen deposition, mRNA expression of PIIIP-alpha1 and TGF-beta1, protein expression of iNOS and TXS, and production of TXA2 in liver perfusates were significantly decreased in UDCA-treated BDL rats. The increased levels of hepatic GSH and SOD activity and decreased levels of TBARS and nitrite were also observed in UDCA-treated BDL rats. In UDCA-treated BDL rats, the reduction in portal pressure resulted from a decrease in IHR, which mostly acted through the suppression of hepatic TXA2 production and lipid peroxidation, and an increase in antioxidative defence, leading to the prevention of hepatic fibrosis.

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Section: Figure 6 Representative Histology Sections Of Livers From Bdsupporting

confidence: 55%

Section: Figure 6 Representative Histology Sections Of Livers From Bdmentioning

confidence: 95%

Section: Figure 6 Representative Histology Sections Of Livers From Bdmentioning

confidence: 96%

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Chronic administration of ursodeoxycholic acid decreases portal pressure in rats with biliary cirrhosis

Yang

Huang²,

Lee

et al. 2008

Clinical Science

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“…There was a positive correlation between these protective effects of GdCl 3 and inhibition of NO production. However, Muriel (1998) demonstrated that AG aggravated CCl 4 -induced hepatic injury, and Wei et al (2005) found that AG improved liver function by its ability to increase hepatic NOS activity in rats. Moreover, Kupffer 's cells has been shown to have a protective role in APAP-induced hepatic injury in mice (Ju et al, 2002) and GdCl 3 was found to produce insignificant effect on APAP-induced hepatotoxicity (Knight and Jaeschke, 2004).…”

Section: Introductionmentioning

confidence: 97%

Role of nitric oxide and reduced glutathione in the protective effects of aminoguanidine, gadolinium chloride and oleanolic acid against acetaminophen-induced hepatic and renal damage

Abdel-Zaher¹,

Abdel-Rahman²,

Hafez³

et al. 2007

Toxicology

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“…Data from animal models of fibrosis or NASH-related liver fibrosis have shown conflicting results of both beneficial and deleterious effects of iNOS. [12][13][14][15][16][17][18][19] The exact reason/s for these paradoxical effects is difficult to explain. Therefore, the present study was undertaken to elucidate the role of iNOS in the pathophysiology of liver fibrosis due to consumption of a HCD.…”

mentioning

confidence: 99%

The role of iNOS in cholesterol-induced liver fibrosis

Anavi

Eisenberg-Bord

Hahn-Obercyger

et al. 2015

Laboratory Investigation

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Accumulation of cholesterol in the liver is associated with the development of non-alcoholic steatohepatitis-related fibrosis. However, underlying mechanisms are not well understood. The present study investigated the role of inducible nitric oxide synthase (iNOS) in cholesterol-induced liver fibrosis by feeding wild-type (WT) and iNOS-deficient mice with control or high-cholesterol diet (HCD) for 6 weeks. WT mice fed with HCD developed greater liver fibrosis, compared with iNOS-deficient mice, as evident by Sirius red staining and higher expression levels of profibrotic genes. Enhanced liver fibrosis in the presence of iNOS was associated with hypoxia-inducible factor-1a stabilization, matrix metalloproteinase-9 expression, and enhanced hepatic DNA damage. The profibrotic role of iNOS was also demonstrated in vivo using a selective inhibitor of iNOS as well as in vitro in a rat liver stellate cell line (HSC-T6). In conclusion, these findings suggest that iNOS is an important mediator in HCD-induced liver fibrosis.Laboratory Investigation (2015) 95, 914-924;

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Chronic administration of aminoguanidine reduces vascular nitric oxide production and attenuates liver damage in bile duct‐ligated rats

Cited by 18 publications

References 44 publications

Chronic administration of ursodeoxycholic acid decreases portal pressure in rats with biliary cirrhosis

Chronic administration of ursodeoxycholic acid decreases portal pressure in rats with biliary cirrhosis

Role of nitric oxide and reduced glutathione in the protective effects of aminoguanidine, gadolinium chloride and oleanolic acid against acetaminophen-induced hepatic and renal damage

The role of iNOS in cholesterol-induced liver fibrosis

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