| OBJECTIVE: To investigate protective effects and mechanisms of astragaloside IV on myocardium injury caused by free radicals.METHODS: Adriamycin (ADR) was administered intraperitoneally to establish the model of myocardium injury caused by oxygen free radicals in rats. Experiments were performed in vivo and in vitro, respectively. In vivo experiments: rats were divided into three groups randomly: the model group (ADR group) received ADR (4.5 mg/kg) intraperitoneally for 2 days; the prophylaxes group (ADR±AST group) received same dose of ADR 30 minutes after being treated with astragaloside IV (AST) (2.0 mg/kg) every day for 2 days; the control group received normal saline (1 ml/kg) intraperitoneally in stead of drugs for 2 days. On the fifth day after treatment with drugs, content of MDA and activity of SOD in myocardium tissue were measured. Ultrastructure of ventricular muscle was observed under the electronic microscope. In vitro experiments: myocytes of new-born rats were incubated with ADR (0.5mg/L and 1.0 mg/L) for 24 hour to induce oxygen free radical injury in model group; same dose of ADR was administered 1 hour after treatment with AST (10 mg/L and 20 mg/L) in therapeutic group and incubated for another 24 hours. Metabolic rate of MTT, content of MDA, activity of NOS, and intracellular free calcium of cardiac myocyte were measured.RESULTS: Experiment in vivo1. Content of MDA: Compared with that of control group (1.39±0.25 nmol/mg protein) , the content of MDA was increased in ADR group (1.88±0.42 nmol/mgprotein), (p<0.05). Compared with that of model group, the content of MDA was decreased in ADR±AST group (1.32 ±0.36 nmol/mg protein), (p<0.05).2. Activity of SOD: Compared with that of control group (33.0 ± 3.21 U/mg protein), the activities of SOD were increased significantly both in ADR group(36.5 ±1.97 U/mg protein) and in ADR±AST group (36.39 ± 3.12 U/mg protein), QK0.05).3. Ultrastructure of myocardium: Hyperplasia, twisting, deformation of myocardial mitochondria, T-tube dilation, interstitial edema, microvessel spasm of myocardium were showed under the electronic microscope, while the above pathologic alterations were attenuated in ADR±AST group.In vitro experiment1. Metabolic rate of MTT: Compared with that of control group (100.0±0%), metabolic rates of MTT was decreased in ADR 0.5 mg/L and 1.0 mg/L groups in a dose dependent manner significantly (60.74 ± 10.63%, 55. 99 ±4.04% ), (PO.01). Compared with that of control group, metabolic rates of MTT in both the small and the large dosage of AST were 94.73 ±9.48%, 96.1 8 ±6.39 respectively (p>0.05). However, the metabolic rate of MTT in cardiac myocyte injured by ADR could be increased. Under the condition that the dosages of ADR were the same, metabolic rate of MTT in the large dosage of AST was increased much more significantly.2. Content of MDA: Compared with that of control group (5 .77 ±1.43 nmol/mg protein), the content of MDA was increased in ADR group (9.65 ±1.43 nmol/mg protein), (p<0.05). Compared with that of ADR group, the content of MDA was dose-dependently decreased in AST 10 mg/L and 20 mg/L groups significantly (6.73 ±2.84 nmol/mg protein, 3.84±0.87 nmol/mg protein), (p<0.05).
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