Study On Mechanism Of Regulating Inflamatory Reaction Of Experimental Vascular Dementia ModeRats With Bu Shen Xing Nao Prescription (BSXNP)

Objective:To observe the BSXNP's influence on the relationship between VD model rat learning and memory,a brain biopsy morphology, and brain inflammatory cells factor TNF-α, IL-1β, IL-10, TGF-β, adhesion molecule ICAM-1, VCAM-1, P-selectin,E-selectin, and the influence on the change of the NF-κB; to study the inflammatory response in rats;to have a further discussing of the regulation function mechanism of action BSXNP prevention VD through the copy of repeatability ischemia-reperfusion.Methods:The first part:the BSXNP's influence on the VD model of rats brain biopsy ethology and morphological.The experiment regard the repeated ischemia-reperfusion cause VD rat models as research object, regard the the joy of as control group, the male Wistar rat randomly is divided into model group (MX), jiaShouShu group (JS), XiDeZhen group (XD), Bu Shen Xing Nao Prescription group (BX), using the diving platform method and water maze method to observe the learning and memory capacity of rats in each group after the experiment respectively in the time of postoperative 7d, 15d,30d. On the second day of the finish of the experiment behaviouristics, bufo by rats organization, take each rats HE dyed observation histopathological morphological changes. Part2:the resistance inhibitory effect of the BSXNP to the inflammatory response of the rat models.The experiment regard the repeated ischemia-reperfusion cause VD rat models as research object, the joy of as control group, divided the male Wistar rat randomly into MX, JS, XD, BX,24hours after the operation, take out the brain by using ELISA take brain test inflammatory cells factor TNF-α, IL-1β, IL-10, TGF-β, adhesion molecule ICAM-1, VCAM-1, P-selectin E-selectin content, using colorimetric detection CHAT, AchE vigor, use protein imprinting method to detect NF-κB expression.Results:The first part:the influence of BSXNP on the VD model of rats brain biopsy ethology and morphological1. BSXNP can improve obviously the VD model rats learning and memory capacity obviously. BSXNP can shrink the response time of VD rat models in different period of the platform experiment obviously, extended the time of electric shock reaction (P<0.01). In the same time, it can also reduce times of the fault reaction in the learning and remembering grade of the VD rat model in the different period (P<0.01). It can also shorten VD model rat'time of searching platform in the Morris water maze and increase the times of acrossing platforms(P<0.01 or P<0.05). And BSXNP group's obviously superior to the group, starwood a statistically significant difference (P<0.05). 2. BSXNP can significantly improve or mitigate the injury of the VD model rats's neurons organizational and BSXNP has a protective effect of the brain nerve cells.Part 2:BSXNP has the resistance inhibitory effect on the inflammatory response of the VD rat models.1. BSXNP can significantly reduce VD model rats organization promote inflammation factors TNF alpha, IL-1βcontent (P< 0.05), decreased the content of anti-inflammatory factor IL-10, TGF-βobviously (P<0.05).2. BSXNP can reduce VD model rats organization ICAM-1, adhesion molecules VCAM-1, E-selectin, P-selectin content in different degree (P<0.01 or P<0.05), and lighten the injury of the chemia-reperfusion.3. BSXNP can improve the activity of ChAT of VD model rats (P<0.05), reducing the activity of AchE (P<0.01), suggesting that its may also play a role in the vagus nerve-choline can anti-inflammatory pathways, VD model rats by dampening the vagus nerve, inhibiting effect by increasing, reduce the synthesis of Ach, inflammatory reaction and thereby reducing brain dysfunction.4. BSXNP can restrain nuclear transcription factors-κB transcription of activity after the brain ischemia reperfusion, reduce NF-κB expression, blocking inflammation, relieve signal transduction pathways inflammatory lesions. Conclusion:1. BSXNP can obviously improve the VD model rats the ability of learning and memory in, reduce the damage of brain neurons, protectie effect of nerve cells.2. This study shows that, after the repeated cerebral ischemia and reperfusion, the inflammatory factor expression rising rapidly, endothelial cell adhesion molecules, choline increased, the anti-inflammatory pathways were not be activated, nuclear transcription factors become active and lead to damage of brain. BSXNP be given to pathways which can block the inflammatory reaction signal, and thus can alleviate inflammation damage. This shows that cerebral ischemia reperfusion appeared after the leucocyte and endothelial cell adhesion, inflammatory cell aggregates, infiltration, inflammation is aggravating, such is its organization capillaries congestion through regulation, one of the pathology base after cerebral ischemia and reperfusion BSXNP treatment early inflammatory reaction is one of the important role the mechanism.Its possible mechanism is: BSXNP by blocking NF-κB inflammatory reaction signalling pathways, and activate the choline can anti-inflammatory pathways, thus common adjust inflammatory factor and adhesion factor expression through multiple access, more and more targets, in the role of inflammatory pathways and link to realize regulation of the inflammatory response function.