| Vascular Dementia(VD),characterized as memory loss and cognitive dysfunction,is a syndrome caused by extensive or focal brain dysfunction resulting from stroke orother various cerebrovascular disease like chronic cerebral ischemic. With agingpopulation, the incidence of VD also increases year by year, which poses a heavyburden on individuals, families and society. At present, drugs used to treat VD mainlyinclude cholinesterase inhibitors, improving cerebral circulation drugs and neuronprotection medicine, etc. Drugs used to treat VD are limited for application because ofside effects or expensive cost. Therefore, finding high potency and low toxicity drugsis an important task for pharmacy workers.Using modern technology, XueShuanXinMaiNing(XSXMN) is made up bydozens of authentic and precious medicines, including salvia root, Maodongqing,leeches, sophora japonica, musk, borneol, bezoar, ginsenosides, toad and so on. Atpresent, it is widely used for cerebral infarction, coronary heart disease and angina inclinical. Plenty of studies have shown that XSXMN has good effect on anti-freeradical oxidative damage, can decrease MDA content, improve circulation, inhibitthrombosis and so on, of which mechanism is closely related to VD pathogenesis.There are no reports on whether XSXMN has therapeutic effects on vasculardementia.VD model was made by bilateral carotid artery occlusion (2-VO). Rats wereintragastric administration for8weeks (XSXMN low dose group1.10g/kg, XSXMNhigh dose group2.20g/kg). By behavior test(water maze and avoid dark), detectingcholinergic system(AchE), free radicals and related enzyme (MDA、SOD、CAT、GSH-Px、Na+-K+-ATPase、Ca2+-Mg2+-ATPase)and pathological examination, weobserved the therapeutic effect on VD rats and explored its mechanism.Compared with the model group: in the Morris water maze, the latency anddistance to platform of rats in low dose group(1.10g/kg) shortened on the2ndand5thday(P<0.01or P<0.05). Starting angle and average velocity to platform had no significant changes from the1stto6thday. In high dose group(2.20g/kg); the latencyto platform decreased from the2ndday to the6thday(P<0.05); The distance toplatform shortened from the1stday to the6thday(P<0.05); the average velocity toplatform had no significant change; on the3rdand4thday, the starting angle becamesmaller(P<0.05). On the7thday, in neither low dose group(1.10g/kg) nor high dosegroup(2.20g/kg), times of passing platform, times of passing effective area, time ofstaying on platform, distance of staying on platform, time of staying in effective area,distance of staying in effective area, time of staying on platform/total time, distance ofstaying on platform/total distance, time of staying in effective area/total time anddistance of staying in effective area/total distance had no obvious changes within2minutes.In the avoid dark test, compared with model group, there’s no obvious change inthe latency of VD rats’ passive avoidance errors or error times in XSXMN groups.Compared with model group, cholinesterase activity of rats’ brain tissue inXSXMN low dose group(1.10g/kg) didn’t change significantly; cholinesteraseactivity of rats’ brain tissue in XSXMN high dose group(2.20g/kg) had a tendency toreduce, but there was no statistical significance.In XSXMN low dose group(1.10g/kg), MDA contents and SOD activity of rats’brain tissue didn’t change significantly; in XSXMN high dose group(2.20g/kg) rats’brain tissue, MDA content decreased and SOD activity increasedsignificantly(P<0.05). None of GSH-Px, CAT, Na+-K+-ATPase, Ca2+-Mg2+-ATPaseactivity of rats’ brain tissue in XSXMN groups changed significantly.In the pathology test, the results showed that XSXMN could mitigate the damageof cerebral cortex and hippocampus in VD rats.All above, XSXMN has therapeutic effect on VD rats, of which mechanism ispossibly related to increasing anti-free radical related enzymes to reduce the damage. |
PDF Full Text Request