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Preliminary Study on the Effect and Mechanism of Kangxueshuanyihao

Author: ZhangZuo
Tutor: CuiZhiQing
School: Tianjin Medical University
Course: Pharmacology
Keywords: Antithrombotic No. Ⅰ Fleabane Salvia Borneol Cerebral complications Platelet aggregation
CLC: R285.5
Type: Master's thesis
Year: 2011
Downloads: 56
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Objective: The purpose of this project is to observation the antithrombotic I thrombosis model of experimental animals and blood rheology, microcirculation, platelet aggregation, and to study the role of antithrombotic No. Ⅰ and preliminary explore its mechanism for further The development of the drug to provide a scientific basis. Methods: (1) anti-thrombotic Ⅰ on FeCl3 due to the impact of the rat cerebral complications. Antithrombotic I is divided into three dose groups were 2g crude drug / kg 4g crude drug / kg, 8g Pharmacognostic / kg, positive control drug breviscapine piece 50mg/kg, positive control drug nimodipine 50mg/kg. Rats in each group are seven days in a row gavage, once daily, one hour after the last administration of middle cerebral artery occlusion test resulting in local cerebral infarction (MCAO) observed antithrombotic I MCAO rats behavior, cerebral infarction area of ??brain tissue pathological morphology. (2) antithrombotic I caused by electrical stimulation of the rat in vivo thrombus. Antithrombotic I three dose groups were dose 1g crude drug / kg, 2 g of crude drug / kg, 4g crude drug / kg. Control group aspirin dose 100mg/kg. Daily, were administered orally for 10 consecutive days. Each group after the last administration, 1 hour, current to stimulate formation of blood clots, thrombosis OT (temperature dump time) as indicators thrombosis length as the main observation indicators. (3) antithrombotic I collagen and adrenaline-induced mice thrombus formation. The antithrombotic No. Ⅰ three dose group, were given the the 2g Pharmacognostic / kg 4g crude drug / kg, 8g Pharmacognostic / kg, and a positive control group was given breviscapine film 30mg/kg. Each group were administered orally for five consecutive days, once a day. 1 hour after the last administration, with the thrombus-inducing agent induced thrombosis. Hemiplegia recovery within 15 minutes of mice as observed indicators. (4) antithrombotic I on ADP-induced platelet aggregation. No. antithrombotic I divided into low, medium, and high dose group were given 2g crude drug / kg 4g crude drug / kg, 8g Pharmacognostic / kg, and a positive control group was given breviscapine film 50mg/kg groups for 5 consecutive days gavage, once a day, comparing antithrombotic Ⅰ each dose group, platelet aggregation inhibition rate and the difference of the positive control group, statistical results using the t test. (5) antithrombotic I adrenaline-induced mouse ear microcirculation. Antithrombotic No. Ⅰ three dose groups, respectively 1g crude drug / kg, 2 g of crude drug / kg, 4g crude drug / kg three dose groups, administered orally for five consecutive days, once a day, the positive control group in the test the day of the abdominal cavity single injections hydrochloric acid raceanisodamine 20mg/kg. Of observation the antithrombotic I number hemorheology. Results: (1) anti-thrombotic I No. 2g crude drug / kg and higher doses can be significantly improved MCAO rats, behavioral disorders, while also significantly reduced the MCAO rat infarct area; histopathological visible 8g crude drug / kg high dose group variability, the fewer the number of necrotic cells, large cerebral infarction area decreased, indicating that the preparation of cerebral ischemia, focal cerebral infarction due to behavioral disorders and organic brain lesions have significantly improved, but MCAO rat brain The Index and brain water content there was no significant impact. (2) 1g crude drug / kg and higher dose rat temperature can dump time (OT) extended thrombus length was significantly shorter, and dose-related, indicating that the preparation of electrical stimulation induced in vivo thrombus significantly inhibited. (3) antithrombotic I 8g crude drug / kg, can increase thrombosis hemiplegia recovery in mice, thus indicating the preparation of collagen and adrenaline-induced mice significantly inhibited thrombosis. (4) antithrombotic No. Ⅰ 8g crude drug / kg of the high-dose group rat platelet aggregation inhibition rate was significantly higher than the positive control Breviscapine piece group, show that the preparations have greater improvement in anticoagulation. (5) antithrombotic No. Ⅰ 2g crude drug / kg and higher doses of the mouse ear microarteries and venule diameter increased significantly, the 4g Pharmacognostic / kg also increase the micro-vein blood flow velocity, indicating that the preparations of mouse The pinna microcirculation having significant improvement in function. Conclusion: antithrombotic I can significantly improve FeCl3-induced rat cerebral complications. And having the role of the anti-electric stimulation and a variety of platelet aggregation-inducing agent-induced thrombosis model. Antithrombotic mechanism of action may be related to confront collagen, epinephrine and ADP-induced platelet aggregation. The antithrombotic I also have a role in the expansion of micro-arteriovenous and speed up micro-vein blood flow velocity. This effect may be related to the main component breviscapine play. These two effects may be the basis of antithrombotic I pharmacological prevention of rat cerebral complications.

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