Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease

AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepati...

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Published inWorld journal of gastroenterology : WJG Vol. 20; no. 4; pp. 1079 - 1087
Main Author Wang, Chao
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Co., Limited 28.01.2014
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Abstract AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepatic encephalopathy.Plasma H2S concentrations and portal vein diameters(PVDs)were compared between portal hypertension patients and control participants,as well as between portal hypertension patients with varying degrees of severity.In addition,we established a rabbit hepatic schistosomiasis portal hypertension(SPH)model and analyzed liver morphology,fibrosis grade,plasma and liver tissue H2S concentrations,as well as cystathionineγ-lyase(CSE)activity and phosphorylated extracellular signal-regulated kinase(pERK)1/2,B cell lymphoma(Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells,in addition to their H2S-induced apoptosis rates.RESULTS:In portal hypertension patients,endogenous H2S levels were significantly lower than those in healthy controls.The more severe the disease was,the lower were the H2S plasma levels,which were inversely correlated with PVD and Child-Pugh score.Liver tissue H2S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals,starting at 3 wk,whereas pERK 1/2expressions gradually increased 12-20 wk after SPH model establishment.In portal vein smooth muscle cells,increasing H2S levels led to increased apoptosis,while Bcl-2 and Bcl-XL expression decreased.CONCLUSION:H2S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction,which helps to maintain normal vascular structures.
AbstractList To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.AIMTo investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates.METHODSPortal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates.In portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased.RESULTSIn portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased.H₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.CONCLUSIONH₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.
To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells. Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H₂S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H₂S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H₂S-induced apoptosis rates. In portal hypertension patients, endogenous H₂S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H₂S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H₂S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H₂S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased. H₂S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.
AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle cells.METHODS:Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels,prothrombin time,ascites and hepatic encephalopathy.Plasma H2S concentrations and portal vein diameters(PVDs)were compared between portal hypertension patients and control participants,as well as between portal hypertension patients with varying degrees of severity.In addition,we established a rabbit hepatic schistosomiasis portal hypertension(SPH)model and analyzed liver morphology,fibrosis grade,plasma and liver tissue H2S concentrations,as well as cystathionineγ-lyase(CSE)activity and phosphorylated extracellular signal-regulated kinase(pERK)1/2,B cell lymphoma(Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells,in addition to their H2S-induced apoptosis rates.RESULTS:In portal hypertension patients,endogenous H2S levels were significantly lower than those in healthy controls.The more severe the disease was,the lower were the H2S plasma levels,which were inversely correlated with PVD and Child-Pugh score.Liver tissue H2S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals,starting at 3 wk,whereas pERK 1/2expressions gradually increased 12-20 wk after SPH model establishment.In portal vein smooth muscle cells,increasing H2S levels led to increased apoptosis,while Bcl-2 and Bcl-XL expression decreased.CONCLUSION:H2S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction,which helps to maintain normal vascular structures.
AIM: To investigate the association between endogenous hydrogen sulfide (H 2 S) and portal hypertension as well as its effect on vascular smooth muscle cells. METHODS: Portal hypertension patients were categorized by Child-Pugh score based on bilirubin and albumin levels, prothrombin time, ascites and hepatic encephalopathy. Plasma H 2 S concentrations and portal vein diameters (PVDs) were compared between portal hypertension patients and control participants, as well as between portal hypertension patients with varying degrees of severity. In addition, we established a rabbit hepatic schistosomiasis portal hypertension (SPH) model and analyzed liver morphology, fibrosis grade, plasma and liver tissue H 2 S concentrations, as well as cystathionine γ-lyase (CSE) activity and phosphorylated extracellular signal-regulated kinase (pERK)1/2, B cell lymphoma (Bcl)-2 and Bcl-XL expression in portal vein smooth muscle cells, in addition to their H 2 S-induced apoptosis rates. RESULTS: In portal hypertension patients, endogenous H 2 S levels were significantly lower than those in healthy controls. The more severe the disease was, the lower were the H 2 S plasma levels, which were inversely correlated with PVD and Child-Pugh score. Liver tissue H 2 S concentrations and CSE expression were significantly lower in the SPH rabbit livers compared with the control animals, starting at 3 wk, whereas pERK 1/2 expressions gradually increased 12-20 wk after SPH model establishment. In portal vein smooth muscle cells, increasing H 2 S levels led to increased apoptosis, while Bcl-2 and Bcl-XL expression decreased. CONCLUSION: H 2 S prevents vascular restructuring caused by excessive proliferation of smooth muscle cells via apoptosis induction, which helps to maintain normal vascular structures.
Author Chao Wang Juan Han Liang Xiao Chang-E Jin Dong-Jian Li Zhen Yang
AuthorAffiliation Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Department of Biliary and Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology Department of Surgery and Biological Therapy, Shenzhen Second People’s Hospital the First Affiliated Hospital of Shenzhen University Department of Respiratory Medicine, Shenzhen People’s Hospital
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Keywords Hydrogen sulfide
Cystathionine γ-lyase
B-cell lymphoma-XL
Portal hypertension
B-cell lymphoma-2
pERK 1/2
Apoptosis
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Notes Chao Wang;Juan Han;Liang Xiao;Chang-E Jin;Dong-Jian Li;Zhen Yang;Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology;Department of Biliary and Pancreatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology;Department of Surgery and Biological Therapy, Shenzhen Second People’s Hospital, the First Affiliated Hospital of Shenzhen University;Department of Respiratory Medicine, Shenzhen People’s Hospital
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Author contributions: Wang C, Han J and Xiao L designed the research; Wang C, Han J, Xiao L, Jin CE, Li DJ and Yang Z performed the research; Wang C, Han J, Xiao L and Jin CE analyzed the data; Wang C, Han J and Xiao L wrote the paper.
Correspondence to: Chao Wang, PhD, Department of General Surgery, Tongji Hospital, Tongji Medical College, Science and Technology of Huazhong University, No. 1095, Jiefang Avenue, Wuhan 430030, Hubei Province, China. wangchao75@sina.com
Telephone: +86-27-83663008 Fax: +86-27-83663039
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Snippet AIM:To investigate the association between endogenous hydrogen sulfide(H2S)and portal hypertension as well as its effect on vascular smooth muscle...
To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells. Portal...
To investigate the association between endogenous hydrogen sulfide (H₂S) and portal hypertension as well as its effect on vascular smooth muscle cells.AIMTo...
AIM: To investigate the association between endogenous hydrogen sulfide (H 2 S) and portal hypertension as well as its effect on vascular smooth muscle cells....
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SubjectTerms Adult
Animals
Apoptosis
B-cell
Brief
Case-Control Studies
Cell Proliferation
Cells, Cultured
Disease Models, Animal
Esophagogastric Junction - blood supply
Esophagogastric Junction - metabolism
Female
Humans
Hydrogen Sulfide - blood
hypertension
Hypertension, Portal - blood
Hypertension, Portal - parasitology
Hypertension, Portal - pathology
Liver - metabolism
Liver - pathology
Liver Cirrhosis, Experimental - metabolism
Liver Cirrhosis, Experimental - parasitology
lymphoma-2
Male
Middle Aged
Muscle, Smooth, Vascular - metabolism
Muscle, Smooth, Vascular - pathology
Myocytes, Smooth Muscle - metabolism
Myocytes, Smooth Muscle - pathology
Portal
Portal Vein - metabolism
Portal Vein - pathology
Rabbits
Schistosomiasis - complications
Severity of Illness Index
Time Factors
Title Role of hydrogen sulfide in portal hypertension and esophagogastric junction vascular disease
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