| The ischemic cerebrovascular disease (ICVD) is common disease and frequently- occurring disease, which harms the human life and health. The pathomechanism is very complex, involving a series of time and spatial cascade response. Although we are getting more and more understanding on its mechanism, but there are still very few effective treatment methods.After cerebral ischemia, the energy metabolism is blocked. The reuptaking of glutamic acid, which depends on enough energy, is damaged. Massive glutamic acid concentrates in synaptic space. Excitatory amino acid acceptors in the cellular membrane are activated intensely by excessive glutamic acid in the intercellular space, which cause the excineurotoxicity damage and the calcium overload. Calcium overload and apoptosis are closely related. Calcium overload is considered the final passage of apoptosis.When the cerebral ischemia occurs, vascular endothelial growth factors have multiple protective functions to the nervous system, including the angiopoiesis, the promotion of neurogenesis, neurotrophy and the neuroprotection, and anti-apoptosis. The mechanism of angiopoiesis is essential. VEGF is one kind of mitogens, which has highly specificity on blood vessel endothelial cell. It can play a specifical part in the blood vessel endothelial cell through its acceptor. It can promote blood vessel endothelial cell multiplication, increase the the permeability of capillaries, promote angiopoiesis, which has essential practical value in clinical medicine.The ginseng is one kind of traditional Chinese medicine. It has the functions of antiinflammation, anti-tumor, relieving calcium overload, protection of cardiac muscles and so on. At present we make amounts of research on some monomers, such as Rb1, Re, Rg1 and so on. It,s clear that they have protective function in cerebral ischemia. F group of ginsenoside is one kind of mixture that be discovered recently, is rich in the ginseng stem and leaf, is composed of ginsenoside F1, F2, F3, F5, notoginsenoside Fe (N-Fe), Rg2. The Jilin University Chemistry Institute pharmaceutical chemistry study team discovered that ginseng stem and leaf contained lots of F group of ginsenoside. They were already successfully in extracting, separating, appraising F group of ginsenoside. About the clinical pharmacological of F group of ginsenoside, they already began the study on F group of ginsenoside anti-myocardial ischemia. Their preliminary research discovered that F group of ginsenoside had the effect of improving myocardial ischemia and hypoxia, expanding coronary artery, and increasing blood supply. At present, there are no research on the function and mechanism of ginsenoside monomer F1, F2, F3, F5, N-Fe and mixture F group of ginsenoside in cerebral ischemia, there are only few articles about the function of ginsenoside monomer Rg2. They confirmed that Rg2 can reduce the excitoxicity damage of PC12 cell effectively which is induced by glumatic acid, suppress inflow of the calcium, reduce the lipid peroxidation and lessen expression of apoptosis preprotein calpain and Caspase-3. Based on present research situation, we suppose that F group of ginsenoside has protective function to the cerebral ischemia damage, and conduct the experimental study.The objective of this experiment is exploring therapeutic action and the mechanism of F group of ginsenoside in ischemic cerebrovascular disease through animal experiment and offering experimental basis for its clinical application, providing new way for the treatment of ischemic cerebrovascular disease.Experimental method:Seventy healthy Wistar rats were chosen and randomly divided into sham operated (group A), control group of sodium chloride (group B), little dosages (group C), middle dosages (group D), large dosages (group E). We induced focal cerebral ischemia model in rats by Zea Longa occlusion methods of right middle cerebral artery. The rats of group C, D, E were given different dosages of F ginsenoside (10mg/kg, 15mg/kg, 20mg/kg) by intraperitoneal injection 30 minutes before the operation, 30 minutes and 3 hours after the operation. We measured the volume of the infarction focus by triphenyl tetrazolium chloride (TTC) stain and observe apoptosis by TUNEL stain and determine the expression of VEGF by immunohis- tochemistry stain.Experimental result:(1) HE staining: Compared with the control group of sodium chloride, the extent of infarction in administration group was decreased, the numbers of remaining nerve cells were more, the extent of nerve cells edema were light, the ischemic change was lighter than in the sodium chloride control group.(2) The infarction volume of the groups which given the drug were smaller (P<0.05). The differences of infarction volume among three group of given drug were not obvious (P>0.05).(3) The number of apoptosis cell of the groups given the drug were reducing, and in experimental dose extent, the numbers of positive cells were smaller following the raise of the medicine dosage.(4) The groups which given the drug compare with the control group of sodium chloride, the expression of VEGF were more obviously, and in experimental dose extent, it expressed more and more following the raise of the medicine dose.Experimental conclusion(1) F group of ginsenoside has the protective function to the cerebral ischemia damage. Compared with the control group, we find out that F group of ginsenoside can lighten the infarction volume.(2) Compared with the giving medicine group and the control group, we find that in the process of focal cerebral ischemia, the F group of ginsenoside can reduce apoptosis of neurons.(3) We confirm that the expression of vascular endothelial growth factor are increase in number at earlier period after focal cerebral ischemia. The expression of VEGF in the medicine groups are higher than the control group obviously. It can provide us a theory base for researching the mechanism of neuroprotection after cerebral ischemia.Through this experiment we confirm that F group of ginsenoside has protective function to the cerebral ischemia damage, the mechanisms contain reducing cell apoptosis, promoting expression of VEGF. It provides a new way for the treatment of ischemic cerebrovascular disease. But because the groups of different dosage of drugs are few in this experiment, we are fail to find the best medicative dosage of F group of ginsenoside in cerebral infarction, it needs us to explore further.
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