[Effects of dl-3-n-butylphthalide on expression of VEGF and bFGF in rat brain with permanent focal cerebral ischemia].

OBJECTIVE: To study the effects of dl-3n-butylphthalide (NBP) on the protein and mRNA expression of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in rats brain with permanent middle cerebral artery occlusion (MCAO). METHODS: The model of permanent MCAO was established by using the suture method of Longa, with which the nylon suture was used to make rat middle cerebral artery (MCA) blocked. Sham-operated rats (n=20) were prepared in similar fashion, but without doing the closed occlusion of the MCA. Operated rats were randomizely divided into model control and NBP groups (n= 20 for each). By intragastric administration, sham-operated and model control group rats were given vegetable oil 2 mL twice daily for 3 days, and also NBP group rats were given NBP 25 mg/kg twice daily for 3 days. The infarct volume and neurological deficit scores were determined by tetrazolium chloride (TTC) staining and Longa's score separately. The protein and mRNA of VEGF and bFGF were detected by immunohistochemistry and in situ hybridization. RESULTS: NBP markedly inhibited the neurological deficit and reduced the infarct volumes as compared to model control group (P < 0.05). NBP significantly upregulated VEGF and bFGF expression in both protein and mRNA levels in the peripheral infarct and hippocampus regions in contrast with sham-operated and model control groups (P < 0.05). In the infarct core, the protein and mRNA levels of VEGF and bFGF did not show significantly any difference (P > 0.05). CONCLUSION: NBP can significantly reduce neurological deficit and infarction volume, and therefore may have protective effect for cerebral ischemia through upregulating the expression of VEGF and bFGF.

[The effect of butylphthalide on expression of NGF and BDNF in ischemia stroke tissue of rat cerebrum].

OBJECTIVE: To study the expressions of BDNF, BDNF mRNA, NGF and NGF mRNA in the permanent focal cerebral ischemia tissues of rats. METHHODS: Healthy male Sprague-Dawley rats were taken for this study project. According to the procedure of Zea-Longa, the rat model with permanent cerebral ischemia was established by rat middle cerebral artery obstructed (MCAO) with a nylon thread, and the model rats of neurobehavioral evaluation as 1-3 grade were randomly divided into two groups: butylphthalide group (A group) and control group (B group). A group was given with 25 mg/kg butylphthalide, B group was given with edible oil, two times every day. 3 days after occlusion, all rats were sacrificed after evaluated the neurobehavioral scores, and the samples of cerebrum were obtained after in situ perfusion and fixation with 40 g/L paraformaldehyde. 5 rats in each group were taken to tetrazolium chloride (TTC) staining for macroscopic observation of cerebral infarction area, the rest samples were processed by immunohistochemistry to evaluate effects of butylphthalide on BDNF and NGF expression, hybridization in situ to evaluate effects of butylphthalide on BDNF mRNA and NGF mRNA expression. SPSS12. 0 for statistical analysis, it was P<0. 05 as having statistical significance. RESULTS: Comparing to control group (B group), butylphthalide group (A group) did not have significantly pathological difference, but the grade of behavior and infarction area were apparently reduced (P<0. 05). In butylphthalide group, there was a significant expression up-regulation to BDNF, NGF, BDNF mRNA and NGF mRNA in the peripheral around infarction and cornu ammonis or hippocampus area (P<0. 05). However in the infarction area, the expressions of BDNF, NGF, BDNF mRNA and NGF mRNA had no significantly statistical difference (P> 0. 05). CONCLUSION: Comparing to control group, butylphthalide can significantly up-regulate the expressions of BDNF and NGF in genetic transcription level, and protect from the ischemia injury.

[Effect of dachuanxiongwan on the expression of vascular epithelial growth factor in rats with cerebral ischemia].

OBJECTIVE: To study the effect of Dachuanxiongwan on the expression of vascular epithelial growth factor in the rats after focal cerebral ischemia and reperfusion. METHODS: The ischemia and reperfusion model was established by blocking the middle cerebral artery of the rats with a nylon thread for two hours. Twenty male Sprague-Dawley rats with middle cerebral artery occlusion (MCAO) were randomly divided into two groups. One of the group of rats were administered with DCXW, 4.13 g/kg x d, twice a day for 3 days by gavaging, while other group were given the same volume of saline as a control. Seventy-two hours after reperfusion, the neuropathological function of the rats were evaluated according to Longa. The rats were then sacrificed and the samples of cerebrum were processed and embedded in paraffin and cut into sections. The expression of VEGF was determined by immunocytochemistry. RESULTS: The score of the neuropathological function of the DCXW treated group (1.5 +/- 0.71) was lower than that of the control group (2.3 +/- 0.82, P = 0.032). More VEGF-positive cells were found in the rats treated with DCXW than those in the control group (P = 0.000). CONCLUSION: DCXW upgrades the expression of VEGF and may have a positive effect on the cerebrum following ischemia and reperfusion.

[A study on the protective efficacy of magnesium against anoxic damage to cultured neurons of rats].

OBJECTIVE: This is an in vitro study aimed to assess the influence of magnesium on cultured anoxic cortical neurons of rats. METHODS: After being treated with MgSO4 and Mg(2+)-ATP respectively, the cortical neurons of rats were given mixture of 97.5% N2 and 2.5% CO2 continuously to set up the model of anoxic cortical neuron of rats at different time points. The mortality of neurons, the levels of Ca2+ within nerve cells (marked by Fluo-3, detected by laser confocal microscopy), and the levels of lactate dehydrogenase (LDH), K+ and neuron specific enolase (NSE) in the culture fluid were investigated at 1,2,4 hours after the inception of anoxia. RESULTS: MgSO4 and Mg(2+)-ATP reduced the calcium influx of anoxic cortical neuron (P<0.05), lowered the level of LDH, K+, NSE in the culture fluid (P<0.05) and significantly decreased the mortality of neurons (P <0.05). CONCLUSION: The protective efficacy of magnesium against the anoxic damage to cultured cortical neurons of rats is corroborated.