Effects of shark hepatic stimulator substance on the function and antioxidant capacity of liver mitochondria in an animal model of acute liver injury
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作者:
Fan, QL
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机构:E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Fan, QL
Huang, CG
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E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R ChinaE China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Huang, CG
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Jin, Y
Feng, B
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机构:E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Feng, B
Miao, HN
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机构:E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Miao, HN
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Li, WJ
Jiao, BH
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机构:E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Jiao, BH
Yuan, QS
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机构:E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
Yuan, QS
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[1] E China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China
[2] Second Mil Med Univ, Dept Biochem & Mol Biol, Shanghai 200433, Peoples R China
This study was carried out to investigate whether shark hepatic stimulator substance (HSS) can prevent acute liver injury and affect mitochondrial function and antioxidant defenses in a rat model of thioacetamide (TAA)-induced liver injury. The acute liver injury was induced by two intraperitoneal injections of TAA (400 mg/kg) in a 24 h interval. In the TAA plus shark HSS group, rats were treated with shark HSS (80 mg/kg) I h prior to each TAA injection. In this group, serum liver enzyme activities were significantly lower than those in the TAA group. The mitochondrial respiratory control ratio was improved, and the mitochondrial respiratory enzyme activities were increased in the TAA plus shark HSS group. The mitochondrial antioxidant enzyme activities and glutathione level were higher in the TAA plus shark HSS group than in the TAA group. These results suggest that the protective effect of shark HSS against TAA-induced acute liver injury may be a result of the restoration of the mitochondrial respiratory function and antioxidant defenses and decreased oxygen stress.
机构:
UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO
AguilarDelfin, I
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LopezBarrera, F
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UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO
LopezBarrera, F
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HernandezMunoz, R
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UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO
机构:
UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO
AguilarDelfin, I
;
LopezBarrera, F
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机构:
UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO
LopezBarrera, F
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HernandezMunoz, R
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UNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICOUNIV NACL AUTONOMA MEXICO,INST FISIOL CELULAR,DEPT BIOENERGET,MEXICO CITY 04510,DF,MEXICO