The Experts below are selected from a list of 657 Experts worldwide ranked by ideXlab platform
Ying Zhang - One of the best experts on this subject based on the ideXlab platform.
-
the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
European Journal of Pharmacology, 2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75mg/kg) and Rifampicin (150mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150mg/kg) 30min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3-nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti-apoptotic effects.
-
pulmonary gastrointestinal and urogenital pharmacology the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:article i nfo Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75 mg/kg) and Rifampicin (150 mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150 mg/kg) 30 min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3- nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti- apoptotic effects.
Xi Chen - One of the best experts on this subject based on the ideXlab platform.
-
the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
European Journal of Pharmacology, 2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75mg/kg) and Rifampicin (150mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150mg/kg) 30min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3-nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti-apoptotic effects.
-
pulmonary gastrointestinal and urogenital pharmacology the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:article i nfo Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75 mg/kg) and Rifampicin (150 mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150 mg/kg) 30 min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3- nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti- apoptotic effects.
Andreas Kuznik - One of the best experts on this subject based on the ideXlab platform.
-
Rifampicin for continuation phase tuberculosis treatment in Uganda: a cost-effectiveness analysis.
PloS one, 2012Co-Authors: Yukari C. Manabe, Sabine Hermans, Mohammed Lamorde, Barbara Castelnuovo, C. Daniel Mullins, Andreas KuznikAbstract:Background In Uganda, Isoniazid Plus ethambutol is used for 6 months (6HE) during the continuation treatment phase of new tuberculosis (TB) cases. However, the World Health Organization (WHO) recommends using Isoniazid Plus Rifampicin for 4 months (4HR) instead of 6HE. We compared the impact of a continuation phase using 6HE or 4HR on total cost and expected mortality from the perspective of the Ugandan national health system. Methodology/Principal Findings Treatment costs and outcomes were determined by decision analysis. Median daily drug price was US$0.115 for HR and US$0.069 for HE. TB treatment failure or relapse and mortality rates associated with 6HE vs. 4HR were obtained from randomized trials and systematic reviews for HIV-negative (46% of TB cases; failure/relapse –6HE: 10.4% vs. 4HR: 5.2%; mortality –6HE: 5.6% vs. 4HR: 3.5%) and HIV-positive patients (54% of TB cases; failure or relapse –6HE: 13.7% vs. 4HR: 12.4%; mortality –6HE: 16.6% vs. 4HR: 10.5%). When the initial treatment is not successful, retreatment involves an additional 8-month drug-regimen at a cost of $110.70. The model predicted a mortality rate of 13.3% for patients treated with 6HE and 8.8% for 4HR; average treatment cost per patient was predicted at $26.07 for 6HE and $23.64 for 4HR. These results were robust to the inclusion of MDR-TB as an additional outcome after treatment failure or relapse. Conclusions/Significance Combination therapy with 4HR in the continuation phase dominates 6HE as it is associated with both lower expected costs and lower expected mortality. These data support the WHO recommendation to transition to a continuation phase comprising 4HR.
Cheng Zhang - One of the best experts on this subject based on the ideXlab platform.
-
the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
European Journal of Pharmacology, 2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75mg/kg) and Rifampicin (150mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150mg/kg) 30min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3-nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti-apoptotic effects.
-
pulmonary gastrointestinal and urogenital pharmacology the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:article i nfo Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75 mg/kg) and Rifampicin (150 mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150 mg/kg) 30 min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3- nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti- apoptotic effects.
Hua Wang - One of the best experts on this subject based on the ideXlab platform.
-
the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
European Journal of Pharmacology, 2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75mg/kg) and Rifampicin (150mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150mg/kg) 30min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3-nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti-apoptotic effects.
-
pulmonary gastrointestinal and urogenital pharmacology the protective effects of ursodeoxycholic acid on Isoniazid Plus Rifampicin induced liver injury in mice
2011Co-Authors: Xi Chen, Cheng Zhang, Hua Wang, Mei Zhao, Zihao Duan, Ying ZhangAbstract:article i nfo Antitubercular drugs have been known to be potentially hepatotoxic and may lead to drug-induced liver injury. In this study, we aimed to investigate the protective effects of ursodeoxycholic acid (UDCA) on liver injury caused by co-administration with Isoniazid and Rifampicin, two famous antitubercular drugs. Liver injury was induced by co-treatment with Isoniazid (75 mg/kg) and Rifampicin (150 mg/kg) for one week. Mice were orally administered with UDCA (15, 50 and 150 mg/kg) 30 min before Isoniazid and Rifampicin. We show that serum alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were significantly increased in mice treated with Isoniazid Plus Rifampicin. An obvious fatty accumulation, accompanied by mild necrosis and inflammation, was observed in liver of mice treated with Rifampicin Plus Isoniazid. In addition, Isoniazid Plus Rifampicin resulted in hepatic apoptosis, as determined by terminal dUTP nick-end labeling (TUNEL) staining and caspase-3 activation. Additional experiment showed that Isoniazid Plus Rifampicin significantly increased the level of hepatic malondialdehyde (MDA) and caused glutathione (GSH) depletion and 3- nitrotyrosine (3-NT) residues in liver. UDCA pretreatment significantly attenuated Isoniazid Plus Rifampicin induced oxidative stress in liver. Importantly, UDCA pretreatment significantly alleviated Isoniazid Plus Rifampicin induced hepatic apoptosis. Moreover, UDCA-mediated anti-apoptotic effect seemed to be associated with its regulation of Bcl-2 and Bax gene expression in liver. These findings suggest that UDCA might protect against Isoniazid and Rifampicin induced liver injury through its anti-oxidative and anti- apoptotic effects.
