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出 处:《Chinese Journal of Traumatology》2000年第4期234-237,共4页中华创伤杂志(英文版)
摘 要:To observe effect of endothelin-1 (ET-1) on hepatic damage induced by endotoxin. Methods: A total of 90 rats were randomly divided into control group (group C), endotoxin treated group (group LPS) and endotoxin plus ET-1 antibody treated group (group LEA). An observation was done on the changes of ET-1 concentration, and transcription and expression of ET-1 mRNA. Plasma glutamic pyruvic-transaminase enzyme (GPT), hepatic lactate dehydrogenase (LDH), adenosine triphosphate (ATP) and malondialdehyde (MDA) were also observed at 3, 6, 9, 12, 24 hours after saline, endotoxin (10 mg·kg -1 ) and ET-1 antibody (dalubine 1: 2*!000 , 2 ml·kg -1 ) administration. Results: The results indicated that the concentration of plasma and hepatic ET-1 and expression of ET-1 mRNA in liver significantly increased following endotoxemia. The hepatic ET-1 levels were inversely correlated with the ATP concentration, and positively related to the MDA concentration. ET-1 antibody could partially protect the liver against damage induced by endotoxin. Conclusions: These results suggest that endotoxin may, on transcription and translation level, lead to an increase of ET-1 in synthesis. ET-1 may contribute to hepatic damage during endotoxemia.To observe effect of endothelin-1 (ET-1) on hepatic damage induced by endotoxin. Methods: A total of 90 rats were randomly divided into control group (group C), endotoxin treated group (group LPS) and endotoxin plus ET-1 antibody treated group (group LEA). An observation was done on the changes of ET-1 concentration, and transcription and expression of ET-1 mRNA. Plasma glutamic pyruvic-transaminase enzyme (GPT), hepatic lactate dehydrogenase (LDH), adenosine triphosphate (ATP) and malondialdehyde (MDA) were also observed at 3, 6, 9, 12, 24 hours after saline, endotoxin (10 mg·kg -1 ) and ET-1 antibody (dalubine 1: 2*!000 , 2 ml·kg -1 ) administration. Results: The results indicated that the concentration of plasma and hepatic ET-1 and expression of ET-1 mRNA in liver significantly increased following endotoxemia. The hepatic ET-1 levels were inversely correlated with the ATP concentration, and positively related to the MDA concentration. ET-1 antibody could partially protect the liver against damage induced by endotoxin. Conclusions: These results suggest that endotoxin may, on transcription and translation level, lead to an increase of ET-1 in synthesis. ET-1 may contribute to hepatic damage during endotoxemia.
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