ABSTRACT
ObjectiveTo explore a feasible animal model of dysphagia after stroke. MethodsTwenty-two clean Sprague-Dawley rats were randomly divided into normal group (n = 11) and model group (n = 11). The model of dysphagia after stroke was established by the thread embolism, and the normal group received no intervention. The latency of the first swallowing attack and the number of swallowing were recorded three and seven days after modeling. The cerebral infarction was detected by TTC staining, and the neuronal apoptosis in ischemic brain was detected by TUNEL fluorescence staining. ResultsCompared with the normal group, the swallowing latency prolonged and the number of swallowing reduced three days in the model group, however, there was no significant difference (P > 0.05); seven days after modeling, the swallowing latency prolonged (P < 0.05), and the number of swallowing slightly reduced with little significant difference (P > 0.05). Compared with the normal group, the brain tissue showed obvious infarction area and a large number of apoptotic cells, while the body mass reduced in the model group (P < 0.05). ConclusionThe model rats express some features of dysphagia, which may become a transformation model of dysphagia after stroke.
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Objective The impact of complement Clq on inflammation in beta amyloidstimulated microglia.Methods After the cultured BV-2 microglial cells were treated with 100mg/L beta-amyloid fibers (fAβs),some of them were given C1q,others wcrc given C1q and C1qA.Then,interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) in the supernatant and cell lysate were determined by the sandwich ELISA.Results A significant increase in TNF-α started at giving 50 nmol/L C1q after 100 mg/L fAβs (F =1177.27,P＜ 0.05),while the release of TNF-α was significantly suppressed by using 50 nmol/L C1qA on basis of this(P＜0.05).The level of IL-6 showed no above change.Conclusions C1q may enhance the inflammation of Aβ-induced BV-2 microglia cells and TNF-α may play important role in this effect.
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Objective To study the effects of butylphthalide (NBP) on memory and apoptosis related protein as well as neuronal pathology in hippocampus of vascular dementia (VD) rats. Methods VD model was generated by the permanent occlusion of bilateral common carotid arteries in SD rats to produce the forebran ischemia. Male SD rats were randomly allocated into sham-operation group, VD model group, NBP treatment group and nimodipine treatment group. The function of memory was tested by the Morris water maze. The neuronal pathological changes and the expression of Bcl-2 and Bax proteins in the hippocampus were observed with hematoxylin-eosin (HE) staining and immunohistochemical staining, respectively. Results The impaired memory of VD rats was proved by the lengthened mean escape latency [(78.79±21.93)vs.(16.96±7.44),P＜0.05] and the neuron in hippocampus was severely damaged. The decveased ratio of Bcl-2/Bax resulted from the overexpression of Bax proteins in VD model group versus the sham-operation group [(43.00±6.72)vs.(6.00±1.29),P＜0.05]. The treatment of NBP notably improved the memory function of VD rats and reduced the hippocampus pathological injury (P＜0.05). The expression of Bcl-2 protein raised [(33.14±8.05)vs.(21.81±4.97),P＜0.05] along with reduced expression of Bax protein [(32.93±4.99)vs.(43.00±6.72),P＜0.05] after NBP treatment. However, there was no significant difference in the treatment effects between nimodipine and NBP group (P＞0.05). Conclusions NBP treatment could improve memory of VD rats and reduce the hippocampus pathological lesion by inhibiting the apoptosis related protein.