Objective To study the protective effect of basic fibroblast growth factor ( bFGF ) on endothelial function and structure of the basilar artery of atherosclerotic rats .Methods A total of forty-eight male adult Wister rats were randomly divided into the normal control , the atherosclerosis ( AS) model and the bFGF treatment groups .The AS model group and the bFGF treatment group were injected with a single dose of vitamin D 3 (6 ×105 IU/kg) and loaded with high fat diet for six consecutive weeks .The bFGF (9.5μg/kg, twice one day) was injection into the abdominal cavity after six weeks in the bFGF treatment group for two weeks , and an identical volume saline was given for the AS model group and the normal control group .After eight weeks , all the rats were sacrificed .The relaxation percentages of the isolated basilar artery in response to acetylcholine ( Ach) were detected and the pathological lesions of them were observed under a light microscope .ELISA and colorimetry assayed the content of serum VEGF and basilar arterial nitric oxide ( NO) .The basilar artery was used for primary culture of both vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs). The influence of bFGF on the proliferation vitality of VECs was measured in vitro with MTT assay.TRITC-phalloidin labeling the cytoskeleton microfilament of VSMCs was observed by laser confocal microscopy .Results The early AS plaques were presented after six weeks by hyper lipid foods .Compared with the AS model group , the relaxation percentage of the isolated basilar artery , the content of both serum VEGF and basilar arterial NO in the bFGF treatment group were obviously increased, but the pathologic injury of the basilar artery was significantly decreased (P<0.05).The proliferation vitality of VECs was obviously increased (P<0.05); the cytoskeleton microfilament of VSMCs was of obviously improvement .Conclusion AS may aggravate the basilar arterial injury , but bFGF may efficiently improve the arterial endothelial function and decrease the pathological lesion of the basilar artery in the AS model rats , which may promote the arterial protective effect .

Objective To study the learning and memory abilities together with the morphological changes in astrocyte and neuron in the hippocampal CA3 area in mice induced by chronic cadmium exposure. Methods Twenty Kunming mice aged 4-5 months were selected by Y-maze and randomly divided into two groups. The cadmium exposed group treated with cadmium (CdCl2,2 mg/kg) by subcutaneous injection,twice a week for 3 consecutive months,and the normal control group were injected with the equal dose of saline. The learning and memory abilities were detected by Y-maze after 3 months of treatment. The structure of astrocytes and neurons in CA3 area of hippocampus were observed under light microscope,and the quantitatively analysis was performed by cell morphometric technique. Results Compared with the control group,learning and memory capacity determined by Y-maze test in the cadmium exposed group were lower (P

Objective To observe the sequential ultrastroctural and electrophysiological changes in the sciatic nerve coagulated by a newly-designed microwave antenna. Methods A total of 75 Sprague-Dawley rats were randomly divided into groups A,B and C and irradiated with microwaves at 10,20 or 30 Watts,for 6 seconds to coagulate the left sciatic nerve.Electrophysiological effects and sequential uhrastructural changes were observed on the 0th,2nd,7th,30th and 60th days after coagulation.A static sciatic index was calculated based on measurements of the footprint on the 7th,30thand 60th days after coagulation.Results On the Oth,2nd,7th and 30th days after cpagulation,the static sciatic index,the nerve conduction velocity and the amplitude of the action potentials in groups B and C had decreased significantly compared with those before coagulation.On the 60th day after coagulation.significant recovery was observed in groups A and B,but not in group C.Only mild alteration in uhrastructure was found,and only in group A.The prominent changes in uhrastructure in group B included broken Schwann cell membranes and myelin disintegration.There were severe injuries in group C,including myelin disintegration,cell deformity,coagulative necrosis,axon necrosis,basement membrane necrosis and demyelination.The structure of the sciatic nerve in group B had partially recovered after 60 days,but group C showed no recovery at all. Conclusion Microwave coagulation of a nerve can block its conduction.and even destroy the nerve.Percutaneous microwave coagulation is clinically feasible and call be an alternative treatment for pain.

Objective : To explore the regulatory mechanism of ginsenoside Rb1 on focal cerebral ischemia-reperfusion injury ( CIRI) ． Methods : A total of 60 C57 / BL mice were randomly divided into 6 groups (n = 10) : shamoperated group ，CIRI model group ，ginsenoside Rb1 low －，medium －，and high-dose group and nimodipine (positive control) group．The surgical method was used to construct the focal CIRI mouse model．The neurological function scores and behavioral tests were performed，and Nissl staining was utilized to detect the number of nissl bodies in the hippocampus．The effect of ginsenoside Rb1 on the molecule expression of the Wnt signaling pathway in the hippocampus was detected by qPCR , Western blot and immunohistochemistry assays．The regulatory mechanism of ginsenoside Rb1 was investigated through molecular docking and co-precipitation assays. Results : Compared with the CIRI model group，the addition of ginsenoside Rb1 reduced the neurological function scores of mice (P＜0. 05) ，shortened the time passing the balance beam (P＜0. 05) ，but increased the time entering the correct arm (P＜0. 05) and the swinging time and climbing time of mice (P ＜0. 05 ) ，indicating that ginsenoside Rb1 could effectively resume the function of the nervous system in mice and improve the behavioral ability of model mice．After ginsenoside Rb1 treatment，axis inhibition protein 2 (Axin2) and glycogen synthase kinase-3 β ( GSK- 3 β) in the hippocampus decreased，whereas the expression of Wnt3a，Wnt1 and β-catenin increased． Conclusion The ginsenoside Rb1 can improve neurological function of the CIRI mouse model and increase the number of Nissl bodies in the hippocampus，which is correlated with the activation of the Wnt signaling pathway，and it may be neuroprotective against focal CIRI during stroke treatment.