Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]

Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
The American Society for Pharmacology and Experimental Therapeutics
Published 2018
Publication Date:
2018-10-09
Publisher:
The American Society for Pharmacology and Experimental Therapeutics
Print ISSN:
0022-3565
Electronic ISSN:
1521-0103
Topics:
Medicine
Published by:
_version_ 1836399064256610304
autor Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
beschreibung Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)- α , vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- α concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.
citation_standardnr 6342074
datenlieferant ipn_articles
feed_id 1930
feed_publisher The American Society for Pharmacology and Experimental Therapeutics
feed_publisher_url http://www.aspet.org/
insertion_date 2018-10-09
journaleissn 1521-0103
journalissn 0022-3565
publikationsjahr_anzeige 2018
publikationsjahr_facette 2018
publikationsjahr_intervall 7984:2015-2019
publikationsjahr_sort 2018
publisher The American Society for Pharmacology and Experimental Therapeutics
quelle Journal of Pharmacology and Experimental Therapeutics
relation http://jpet.aspetjournals.org/cgi/content/short/367/2/260?rss=1
search_space articles
shingle_author_1 Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
shingle_author_2 Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
shingle_author_3 Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
shingle_author_4 Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
shingle_catch_all_1 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)- α , vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- α concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.
Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
The American Society for Pharmacology and Experimental Therapeutics
0022-3565
00223565
1521-0103
15210103
shingle_catch_all_2 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)- α , vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- α concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.
Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
The American Society for Pharmacology and Experimental Therapeutics
0022-3565
00223565
1521-0103
15210103
shingle_catch_all_3 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)- α , vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- α concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.
Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
The American Society for Pharmacology and Experimental Therapeutics
0022-3565
00223565
1521-0103
15210103
shingle_catch_all_4 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
Chronic hepatitis is the major cause of liver cirrhosis and portal hypertension. Several factors affect portal pressure, including liver fibrosis, splanchnic vasodilatation, and pathologic angiogenesis. Nucleos(t)ide analogs (NUCs), the oral antiviral agents, effectively attenuate chronic hepatitis B-related liver cirrhosis and portal hypertension via viral suppression and alleviation of hepatitis. On the other hand, NUCs affect tumor necrosis factor (TNF)- α , vascular endothelial growth factor (VEGF), and nitric oxide, which participate in fibrogenesis, vasodilatation, and angiogenesis. However, whether NUCs independently influence liver fibrosis and portal hypertension beyond viral suppression is unknown. This study thus aimed to evaluate the influences of three frequently used NUCs in rats with nonviral cirrhosis. Male Sprague-Dawley rats received common bile duct ligation (CBDL) to induce cholestatic cirrhosis and portal hypertension. The rats were randomly allocated into four groups, treated by mouth with lamivudine (30 mg/kg per day), entecavir (0.09 mg/kg per day), tenofovir (50 mg/kg per day), or distilled water (vehicle control) from the 15th day after CBDL. On the 29th day, liver cirrhosis- and portal hypertension-related parameters were evaluated. The results showed that chronic NUCs treatment did not affect hemodynamic parameters, plasma TNF- α concentration, and hepatic fibrogenesis protein expressions in rats with nonviral cirrhosis. Though the mesenteric VEGF receptor 2 phosphorylation was downregulated in NUCs-treated groups, the splanchnic angiogenesis was not influenced. In conclusion, lamivudine, entecavir, and tenofovir had no additional effects on liver cirrhosis and portal hypertension in rats with nonviral cirrhosis.
Hsieh, Y.-H., Huang, H.-C., Chang, C.-C., Chuang, C.-L., Lee, F.-Y., Hsu, S.-J., Huang, Y.-H., Hou, M.-C., Lee, S.-D.
The American Society for Pharmacology and Experimental Therapeutics
0022-3565
00223565
1521-0103
15210103
shingle_title_1 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
shingle_title_2 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
shingle_title_3 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
shingle_title_4 Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
timestamp 2025-06-30T23:37:02.019Z
titel Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
titel_suche Nucleos(t)ide Analogs Do Not Independently Influence Hepatic Fibrosis and Portal Hypertension beyond Viral Suppression in CBDL-Induced Cirrhotic Rat [Gastrointestinal, Hepatic, Pulmonary, and Renal]
topic WW-YZ
uid ipn_articles_6342074