AIM： The balance between oxidants and antioxidants can play an important role in the initiation and development of liver diseases. Recently, we have described a new automated method for the determination of total ant...AIM： The balance between oxidants and antioxidants can play an important role in the initiation and development of liver diseases. Recently, we have described a new automated method for the determination of total antioxidant capacity （TAC） in human serum and plasma.METHODS： We measured TAC and corrected TAC （CTACabstraction of interactions due to endogenous uric acid,bilirubin and albumin） in 52 patients with chronic liver diseases （41 patients with primary biliary cirrhosis （PBC）,10 patients with chronic hepatitis C and 13 patients with viral HCV cirrhosis） as well as in 10 healthy controls. In 23 PBC patients measurement were also done 6 mo after treatment with ursodeoxycholic acid （UDCA）. The TAC assay was based on a modification of the crocin bleaching assay. The results were correlated with routine laboratory measurements and the histological stage of PBC.RESULTS： There were no significant differences in TAC between the various groups. However, CTAC was considerably increased in the PBC group compared to controls and cirrhotics. Analysis of these patients according to disease stages showed that this increase was an early phenomenon observed only in stages I and II compared to controls, cirrhotics and patients with chronic hepatitis C）.After 6 mo of treatment with UDCA, levels of CTAC decreased to those similar to that of controls.CONCLUSION： Patients in the early stages of PBC present with high levels of corrected total antioxidant capacity and this maybe related to the pathophysiology of the disease. UDCA treatment restores the levels of CTAC to control levels.展开更多
Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ ...Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ damage and therefore accelerate the rate of recovery. In recent years, substantial amounts of data about the efficiency of antioxidants against oxidative damage have been obtained from experiments with rodents. Some of these antioxidants have been found beneficial in the treatment of AP in humans; however, at present there is insufficient clinical data to support the benefits of antioxidants, alone or in combination with conven-tional therapy, in the management of AP in humans. Conflicting results obtained from experimental animals and humans may represent distinct pathophysiological mechanisms mediating tissue injury in different species. Further detailed studies should be done to clarify the exact mechanisms of tissue injury in human AP. Herein I tried to review the existing experimental and clinical studies on AP in order to determine the efficiency of antioxidants. The use of antioxidant enriched nutrition is a potential direction of clinical research in AP given the lack of clues about the efficiency and safety of antioxidant usage in patients with AP.展开更多
AIM:To evaluate whether combination therapy with antitumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis.METHODS:Colitis was induced in CD1-Swiss mice with ...AIM:To evaluate whether combination therapy with antitumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis.METHODS:Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d.The experimental mice were then randomised into the following subgroups:standard diet + DSS treated (induced colitis group);standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group;Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα;standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα.Each group of mice was matched with a similar group of sham control animals.Macroscopic and histological features were scored blindly.Homogenates of the colonic mucosa were assessed for myeloperoxidase activity as a biochemical marker of inflammation and DNA adducts (8OH-dG) as a measure of oxidative damage.RESULTS:DSS produced submucosal erosions,ulcers,inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc.The effect was more pronounced in the latter group (vs Zn diet,P < 0.02).Myeloperoxidase activity (vs controls,P < 0.02) and DNA adducts,greatly elevated in the DSS fed colitis group (vs controls,P < 0.05),were significantly reduced in the treated groups,with a more remarkable effect in the group receiving combined therapy (vs standard diet,P < 0.04).CONCLUSION:DSS induces colonic inflammation which is modulated by the administration of anti-TNFα.Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.展开更多
AIM： To investigate dose-response and time-course of the effects of ethanol on the cell viability and antioxidant capacity in isolated rat hepatocytes. METHODS： Hepatocytes were isolated from male adult Wistar rats ...AIM： To investigate dose-response and time-course of the effects of ethanol on the cell viability and antioxidant capacity in isolated rat hepatocytes. METHODS： Hepatocytes were isolated from male adult Wistar rats and seeded into 100-mm dishes. Hepatocytes were treated with ethanol at concentrations between 0 （C）, 10 （E10）, 50 （E50）, and 100 （E100） mmol/L （dose response） for 12, 24, and 36 h （time course）. Then, lactate dehydrogenase （LDH） leakage, malondialdehyde （IDA） concentration, glutathione （GSH） level, and activities of glutathione peroxidase （GPX）, glutathione reductase （GRD）, superoxide dismutase （SOD）, and catalase （CAT） were measured. RESULTS： Our data revealed that LDH leakage was significantly increased by about 30% in group E100 over those in groups C and E10 at 24 and 36 h, The HDA concentration in groups C, E10 and E50 were significantly lower than that in group E100 at 36 h. Furthermore, the concentration of IDA in group E100 at 36 h was significantly higher by 4.5- and 1.7-fold, respectively, than that at 12 and 24 h. On the other hand, the GSH level in group E100 at 24 and 36 h was significantly decreased, by 32% and 28%, respectively, compared to that at 12 h. The activities of GRD and CAT in group E100 at 36 h were significantly less than those in groups C and E10. However, The GPX and SOD activities showed no significant change in each group. CONCLUSION： These results suggest that longtime incubation with higher concentration of ethanol （100 mmol/L） decreased the cell viability by means of reducing GRD and CAT activities and increasing lipid peroxidation.展开更多
Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet s...Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet supplemented by bovine serum albumin injection bolus. The rabbits were randomly divided into the control, model, and valsartan treated group, six rabbits in each group. Blood samples were collected at the end of 8 weeks for examination of serum lipid levels and MDA levels; the aortas were harvested for histological morphometry analysis, vascular cell adhesion molecule-1 (VCAM-1) immunohistochemical analysis and in situ superoxide detection to reflect the activity of NAD(P)H oxidase. Results: Rabbits fed with high cholesterol diet showed higher serum lipids levels than those fed with normal diet(P<0.01). Treatment with valsartan (10 mg/kg per day) did not alter serum lipids levels. But the serum MDA level and ratio of lesion to intima area reduced significantly compared with model group(P<0.05). The expression of VCAM-1 decreased significantly in the valsartan treated group than in the model group (P<0.05).In addition, in situ superoxide detection also show the markedly reduction of superoxide as a result of valsartan treatment. Conclusion: These results indicate that the valsartan treatment can reduce the atherosclerotic progression, the mechanisms of which may include the inhibiting the NAD(P)H oxidase activity to produce superoxide and the downregulating the expression of redox sensitive genes in the downstream, such as VCAM-1.展开更多
文摘AIM： The balance between oxidants and antioxidants can play an important role in the initiation and development of liver diseases. Recently, we have described a new automated method for the determination of total antioxidant capacity （TAC） in human serum and plasma.METHODS： We measured TAC and corrected TAC （CTACabstraction of interactions due to endogenous uric acid,bilirubin and albumin） in 52 patients with chronic liver diseases （41 patients with primary biliary cirrhosis （PBC）,10 patients with chronic hepatitis C and 13 patients with viral HCV cirrhosis） as well as in 10 healthy controls. In 23 PBC patients measurement were also done 6 mo after treatment with ursodeoxycholic acid （UDCA）. The TAC assay was based on a modification of the crocin bleaching assay. The results were correlated with routine laboratory measurements and the histological stage of PBC.RESULTS： There were no significant differences in TAC between the various groups. However, CTAC was considerably increased in the PBC group compared to controls and cirrhotics. Analysis of these patients according to disease stages showed that this increase was an early phenomenon observed only in stages I and II compared to controls, cirrhotics and patients with chronic hepatitis C）.After 6 mo of treatment with UDCA, levels of CTAC decreased to those similar to that of controls.CONCLUSION： Patients in the early stages of PBC present with high levels of corrected total antioxidant capacity and this maybe related to the pathophysiology of the disease. UDCA treatment restores the levels of CTAC to control levels.
文摘Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ damage and therefore accelerate the rate of recovery. In recent years, substantial amounts of data about the efficiency of antioxidants against oxidative damage have been obtained from experiments with rodents. Some of these antioxidants have been found beneficial in the treatment of AP in humans; however, at present there is insufficient clinical data to support the benefits of antioxidants, alone or in combination with conven-tional therapy, in the management of AP in humans. Conflicting results obtained from experimental animals and humans may represent distinct pathophysiological mechanisms mediating tissue injury in different species. Further detailed studies should be done to clarify the exact mechanisms of tissue injury in human AP. Herein I tried to review the existing experimental and clinical studies on AP in order to determine the efficiency of antioxidants. The use of antioxidant enriched nutrition is a potential direction of clinical research in AP given the lack of clues about the efficiency and safety of antioxidant usage in patients with AP.
文摘AIM:To evaluate whether combination therapy with antitumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis.METHODS:Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d.The experimental mice were then randomised into the following subgroups:standard diet + DSS treated (induced colitis group);standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group;Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα;standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα.Each group of mice was matched with a similar group of sham control animals.Macroscopic and histological features were scored blindly.Homogenates of the colonic mucosa were assessed for myeloperoxidase activity as a biochemical marker of inflammation and DNA adducts (8OH-dG) as a measure of oxidative damage.RESULTS:DSS produced submucosal erosions,ulcers,inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc.The effect was more pronounced in the latter group (vs Zn diet,P < 0.02).Myeloperoxidase activity (vs controls,P < 0.02) and DNA adducts,greatly elevated in the DSS fed colitis group (vs controls,P < 0.05),were significantly reduced in the treated groups,with a more remarkable effect in the group receiving combined therapy (vs standard diet,P < 0.04).CONCLUSION:DSS induces colonic inflammation which is modulated by the administration of anti-TNFα.Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.
基金Supported by the Research Fund from Cathay General Hospital in Taiwan, 93CGH-TMU-15
文摘AIM： To investigate dose-response and time-course of the effects of ethanol on the cell viability and antioxidant capacity in isolated rat hepatocytes. METHODS： Hepatocytes were isolated from male adult Wistar rats and seeded into 100-mm dishes. Hepatocytes were treated with ethanol at concentrations between 0 （C）, 10 （E10）, 50 （E50）, and 100 （E100） mmol/L （dose response） for 12, 24, and 36 h （time course）. Then, lactate dehydrogenase （LDH） leakage, malondialdehyde （IDA） concentration, glutathione （GSH） level, and activities of glutathione peroxidase （GPX）, glutathione reductase （GRD）, superoxide dismutase （SOD）, and catalase （CAT） were measured. RESULTS： Our data revealed that LDH leakage was significantly increased by about 30% in group E100 over those in groups C and E10 at 24 and 36 h, The HDA concentration in groups C, E10 and E50 were significantly lower than that in group E100 at 36 h. Furthermore, the concentration of IDA in group E100 at 36 h was significantly higher by 4.5- and 1.7-fold, respectively, than that at 12 and 24 h. On the other hand, the GSH level in group E100 at 24 and 36 h was significantly decreased, by 32% and 28%, respectively, compared to that at 12 h. The activities of GRD and CAT in group E100 at 36 h were significantly less than those in groups C and E10. However, The GPX and SOD activities showed no significant change in each group. CONCLUSION： These results suggest that longtime incubation with higher concentration of ethanol （100 mmol/L） decreased the cell viability by means of reducing GRD and CAT activities and increasing lipid peroxidation.
文摘Objective: To investigate the therapy effect of valsartan on oxidative stress and the formation of atherosclerosis of rabbit. Methods: An atherosclerotic rabbit model was established by feeding high cholesterol diet supplemented by bovine serum albumin injection bolus. The rabbits were randomly divided into the control, model, and valsartan treated group, six rabbits in each group. Blood samples were collected at the end of 8 weeks for examination of serum lipid levels and MDA levels; the aortas were harvested for histological morphometry analysis, vascular cell adhesion molecule-1 (VCAM-1) immunohistochemical analysis and in situ superoxide detection to reflect the activity of NAD(P)H oxidase. Results: Rabbits fed with high cholesterol diet showed higher serum lipids levels than those fed with normal diet(P<0.01). Treatment with valsartan (10 mg/kg per day) did not alter serum lipids levels. But the serum MDA level and ratio of lesion to intima area reduced significantly compared with model group(P<0.05). The expression of VCAM-1 decreased significantly in the valsartan treated group than in the model group (P<0.05).In addition, in situ superoxide detection also show the markedly reduction of superoxide as a result of valsartan treatment. Conclusion: These results indicate that the valsartan treatment can reduce the atherosclerotic progression, the mechanisms of which may include the inhibiting the NAD(P)H oxidase activity to produce superoxide and the downregulating the expression of redox sensitive genes in the downstream, such as VCAM-1.
