RESUMO
OBJECTIVE: To research the effects of Erigeron breviscapus injection (EBI) on TNF-alpha, PAI-1 and tPA in rats with acute myocardial infarction. METHODS: Models of acute myocardial infarction (AMI)were produced by ligation of left anterior descending coronary artery, then rats were randomly divided into control and experimental groups, then respectively gavaged NS, and the low, middle and high dosage of EBI for one week. The cardiac function index and the expression of TNF-alpha, tPA and PAI-1 were measured. RESULTS: Compared with the NS group, the cardiac function LVEDP, MAP, LVPmax, +/- dp/dt of AMI rat was improved by EBI in all dosage range, and the expression of TNF-alpha and PAI-1, LVEDP were decreased (P < 0.05), the expression of tPA, MAP, LVPmax and +/- dp/dt were increased obviously (P < 0.05) and had a dose-effect relationship. CONCLUSION: EBI can inhibit the expression of TNF-alpha and PAI-1, increase the expression of tPA,which can prevent the ongoing thrombopoiesis after AMI and improve the cardiac function. This maybe attributes to the inhibition of the overexpression of TNF-alpha.
Assuntos
Medicamentos de Ervas Chinesas/farmacologia , Erigeron , Infarto do Miocárdio/tratamento farmacológico , Miocárdio/metabolismo , Inibidor 1 de Ativador de Plasminogênio/metabolismo , Fator de Necrose Tumoral alfa/metabolismo , Doença Aguda , Animais , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Medicamentos de Ervas Chinesas/administração & dosagem , Medicamentos de Ervas Chinesas/uso terapêutico , Erigeron/química , Injeções , Masculino , Infarto do Miocárdio/etiologia , Infarto do Miocárdio/fisiopatologia , Miocárdio/patologia , Inibidor 1 de Ativador de Plasminogênio/sangue , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Ativador de Plasminogênio Tecidual/sangue , Ativador de Plasminogênio Tecidual/metabolismo , Fator de Necrose Tumoral alfa/sangueRESUMO
OBJECTIVE: To research the effects of Panax notoginseng saponins (PNS) on angiotensin-converting enzymes 2 ( ACE2) and tumor necrosis factor-alpha (TNF-alpha) in rats with post-myocardial infarction ventricular remodeling. METHODS: Models of acute myocardial infarction (AMI) were produced by ligation of left anterior descending coronary artery, 24 hours after operation the rats were randomly divided into control and experiment groups, then respectively administrated with NS, fosinopril and low, middle and high dosage of PNS for four consecutive weeks. To observe effects of PNS on malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GSH-Px), ACE2 and TNF-alpha in rats with post-myocardial infarction ventricular remodeling. RESULTS: Compared with NS group, MDA significantly decreased, the activity of GSH-Px significantly increased (P < 0.05 or P < 0.01), NO of the high-dose PNS group decreased (P < 0.05), Compared with the NS group, ACE2 increased and TNF-a significantly decreased in low-dose PNS group, middle and high-dose groups (P < 0.05). CONCLUSION: PNS can stimulate ACE2 to inhibit the expression of TNF-alpha and enhance the antioxidance. PNS can reduce pathological injury of cardiac myocytes in myocardial ischemia and cardiac muscle, which can improve ventricular remodeling.