AIM: To investigate the effects of Scutellaria barbata flavonoids (SBF) on neurofibrillary tangle (NFT) aggregation, tau protein phosphorylation and the regulated mechanism of glycogen synthase kinase (GSK) 3βand protein phosphatase (PP) 2A in the rats induced by amyloid βprotein 25-35 (Aβ25-35) in combination with AlCl3 and re-combinant human transforming growth factor ( RHTGF)-β1( composited Aβ) .METHODS:The male SD rats were used to establish the simulated Alzheimer disease ( AD) model by intracerebroventricular injection of composited Aβ.The Morris water maze was applied for screening the successful model rats with learning and memory deficits .The successful model rats were daily and orally administrated with SBF at doses of 35, 70 and 140 mg/kg or positive control drug Ginkgo biloba leaves flavonoids ( GLF) at 140 mg/kg for 37 d.The silver nitrate staining was used to determine the cortical NFT .The protein levels of total tau, phosphorylated protein of tau at Ser199 and Ser214 sites, GSK3βand PP2A in hippocampus and cortex were determined by Western blot .The mRNA expression of GSK3βand PP2A in the hippocampus and cortex was detected by RT-PCR.RESULTS:Compared with sham group , the cell number of positive NFT with silver nitrate staining in model rat cerebral cortex was significantly increased .The protein levels of phosphorylated tau protein at Ser 199 and Ser214 sites, GSK3βin the hippocampus and cerebral cortex in the model rats dramatically elevated , and PP2A was marked decreased as compared with the sham group rats.Meanwhile, the mRNA expression of GSK-3βsignificantly increased but PP2A was de-creased.However, these above abnormalities were differently attenuated by treating with SBF at different doses or GLF at 140 mg/kg for 37 d.CONCLUSION: SBF suppresses the NFT aggregation by inhibition of the regulatory functions of GSK-3βand PP2A, thus reducing the phosphorylation of tau protein .

Aim To study effects of total flavonoids from stems and leaves of Scutellaria baicalensis Georgi(SSF)on learning and memory deficits, automatic dyskinesia, neural and hepatic pathological changes and free radicals abnormal alterations.Methods Aluminum toxic model of mice was produced by introperitoneal injection (ip) of AlCl_3 for 50 d. Behavioral test of mice was used to examine the learning and memory ability;the number of automatic action determined the automatic dyskinesia;the neural and hepatic pathological changes were assessed by alterations of cerebral cortex and liver;MDA level and SOD activity in brain and liver were measured to evaluate free radicals.Results AlCl_3(100 mg?kg~-1 ,ip,50 d)resulted in a decreased ability of learning and memory in water maze task, lowered automatic action numbers, neuronal-hepatic-pathological changes and free radicals abnormal alterations, as compared with control group. The dose of SSF 50, 100 and 200 mg?kg~-1 significantly reversed the above pathological changes in toxic mice caused by aluminum. Conclusion SSF could reduce cognitive deficits and automatic dyskinesia, improve neuronal-hepatic-pathological changes and free radicals abnormal alterations.

Objective To study the effect of Yuzhenxifeng Decoction on the brain ferritin in PD mouse models .Methods All ex‐perimental animals were devided into 4 groups:the control group ,the model group ,the positive drug group and TCM group .Prepare PD model mice with MPTP ,then use the immunohistochemical staining technique to observe the change of expression of Fn .Results the results showed that compared with the model group ,movement coordination disorder of rats in TCM group were relieved ;the Fn level of the model group on 6th ,13th ,20th were higher than control group(P<0 .05) ,and were 2 .21 times ,1 .15 times and 0 .36 times higher respectively .Compared with model group mice ,expression of Fn were enhanced in the treatment group .Conclusion Yuzhenxifeng Decoction can improve the expression of Fn in the brain ,which provide the basis for further study on mechanism of the treatment of Parkinson′s disease .

Objective To observe the effect on Foxg1 gene expression in the subgranular zone (SGZ) of cerebral tissue from neonatal rats with hypoxic-ischemic brain damage (HIBD) after transplantation of neural stem cells (NSCs) derived from umbilical cord blood.Methods Mononuclear cells separated from umbilical cord blood by density gradient centrifugation were cultured with orientated induction to differentiate the NSCs.The neuronal phenotype was identified using immunocytochemical methods.A total of 150 Sprague-Dawley rats were randomly divided into a sham-operation group,an HIBD group and an HIBD-NSCs group.Rats in the HIBD group and the HIBD-NSCs group were subject to ligation of the left carotid artery and then kept in a box under 8％ oxygen and 92％ nitrogen for 2.5 hours to establish the HIBD animal model.The artery was separated but not ligated in the sham operation group,which was not subjected to hypoxia.Twenty-four hours after the operation,the cultivated NSCs were transplanted by caudal vein injection into the rats in the HIBD-NSCs group.Rats were then sacrificed on the 3rd,7th,14th,21st and 28th days after the operation.Foxg1 gene expression in the SGZ was examined using in-situ hybridization methods.Results The number of Nestin-positive cells peaked on the 6th day of cultivation and then decreased by the 9th day.The Foxg1 gene was expressed in the SGZs of each group.The expression increased by the 3rd day after surgery in the HIBD and HIBD-NSCs groups,and peaked on 7th day after the operation,then declined gradually.The average expression level of Foxg1 in the HIBD group was significantly lower than that in the HIBD-NSCs group on the 7th day and thereafter.Conclusions Human umbilical cord blood mesenchymal stem cells can be induced and differentiated into neural stem cells.Foxg1 genes can still be present in the SGZ after birth.HIBD can induce the expression of Foxg1 genes.Transplanting NSCs can promote the expression of Foxg1 genes and improve morphological and functional recovery after HIBD,at least in neonatal rats.