| AIMFocal brain ischemia/reperfiision can not only save the dying neuron, but also aggravate the neuron damnification and even cause them death. Recent studies show that more and more attentions are taken into the inflammation mechanism involved into focal brain ischemia/reperfusion, in which the importance of the cell factors have been revealed farther . Meanwhile, the traditional medicine-ligustrazine has some roles on treating brain ischemia, which include dilating blood vessel, restrain platelet congregation, improving microcirculation and opposing lipid oxidation. However, no reports are found in the field that whether ligustrazine has the role of brain protection by affecting the metabolism of cell factors. Therefore, for probing into the detail, we applied radioimmunoassay to investigate the effect of ligustrazine on interleukin-6 (IL-6 ) and Tumor necrosis factor-a(TNF-a) expression in different time points after local cerebral ischemia reperfusion, and electron microscope to observe the developing changes of hippocampus CA1 area neurons and astrocytes.Mtheods1. We produced middle cerebral artery occlusion/reperfusion (MCAO) models of SD rats. The rats of experimental group were injected ligustrazine in abdomen, and 0.9%NaCl in control group.2. On separately 5 time points (0.5h after ischemia and Ih, 3h, 6h, 12h during reperfusion), we killed the rats and removed their brains for detecting IL-6 and TNF-a expression by radioimmunoassay.3. Separately on reperfusion 6h and 12h of experimental group and controlgroup, we applied electron microscope to observe the developing changes of hippocampus CA1 area neurons and astrocytes.Results1. Changes of IL-6In control group IL-6 expression were observed at 0.5 h after ischemia, Ih, 3h and 6h after reperfusion, and without any significant difference(P>0.05), while at 12h after reperfusion higher IL-6 expression was found (P>0.05) ; In experimental group the IL-6 expression was obviously increased at 6h after reperfusion compared with the other time points in the same group P>0.05) and the control group (PO.05).2. Changes of TNF-aIncrease was investigated 0.5h after ischemia which continue to improve while reperfusion, reaching the maximum at 12h after reperfusion. The level of TNF-a in animals with ligustrazine treatment were higher than animals in sham-operation group but significantly lower than control animals.3. Changes of ultrastructureUltrastructure changes of hippocampus CA1 area neurons and astrocytes totally were slighter in experimental group than control group. (1) 6h during reperfusion in experimental group: Astrocytes protuberance swelled, but the miotochodrions had unmarked changes. Miotochodrions swelled partly and endoplasmic reticulum expanded in neuron. (2) 12h during reperfusion in experimental group: Astrocytes protuberance swelled, but the miotochodrions had unmarked changes. Miotochodrions swelled and vacuolizated in neuron which were not connected with astrocytes. But in neuron connecting with astrocytes, we found miotochodrions had unmarked changes and onlyendoplasmic reticulum had slight changes. ConclusionTNF-a can aggravate damnification of focal brain ischemia/reperfusion. IL-6 may be a internal antagon which can protect the neuron from death. Ligustrazine can restrain the expression of TNF-ain focal brain ischemia/reperfusion and protect the neuron and astrocytes of hippocampus CA1 area. Simultaneity, ligustrazine can advance the expression of IL-6. This may be one of the mechanisms of ligustrazine protection. |
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