Objective To determine the effect of willed movement on the expression of Nogo-A and Rho-associated kinase (ROCK) in adult rats with cerebral ischemia.Methods Cerebral ischemia/reperfusion injury was established by middle cerebral artery occlusion (MCAO) for 2 h,followed by a 24 h reperfusion in 54 adult rats and the degree of their neurological deficit was evaluated using Longa scale.They were then divided randomly into 3 groups,namely the MCAO group,the environmental modification (EM) group,and the willed movement (WM) group.The rats of MCAO group were raised in a regular breeding box,where they could get food and water freely.Meanwhile,those of the other two groups were raised in a homemade box.For the WM group,the water bottle and food were located on the roof of the homemade box.In each group,six rats were killed on day 3,7 and 15 after reperfusion and their neurological deficits were evaluated respectively.Immunohistochemistry assay was employed to examine the expression of Nogo-A and ROCK in the brain tissue around the ischemic foci.Results The rats of the WM group showed lessened neurological deficits on day 15 compared with the model and EM group.Their expression of Nogo-A decreases from(28.92 ± 2.17)/hpf on day 7 to (24.38 ± 2.29)/hpf on day 15 and that of ROCK did from (40.03 ± 2.14)/hpf to (38.08 ± 2.07) / hpf,lower than those of the model and EM group.However,no significant differences were found in the expression of Nogo-A and ROCK between the model group and EM group at any time points.Conclusion Willed movement could promote the functional recovery of neurological deficits in rats with ischemia after reperfusion,which is probably in relation to restrained expression of Nogo-A and Rho-associated in the tissue around the brain ischemic foci.

Objective To study the effect of Polygonum Multiflorum Thunb(PMT) on learning-memory ability in rats with Alzheimer disease(AD) and its probable mechanism. Metheds Rats were trained by Y-maze and were detected its learning-memory ability before the rats received the injection of A?1-40. The rats were treated with different dosage of PMT after the model of AD was set up. The learning-memory ability and the levels of superoxide dismutase (SOD) and malondialdehyde(MDA) were detected. Results Compared with model rats, the rats treated by middle and high-dosage of PMT, the learning-memory ability of was better,the SOD activity of was higher and the MDA concentration of was lower (P

Objective To study the changes of white matter fiber tracts in mild traumatic brain injury(mTBI)patients by using DTI technique on 3.0T MR system,and evaluate the clinical diagnostic value of DTI.Methods Thirty mTBI and 30 matched health-y controls underwent conventional CT,MRI and DTI examinations.FA values and ADC values in the genu of the corpus callosum, the splenium of the corpus callosum,bilateral internal capsule,the cingulum bundle,the bilateral superior longitudinal fasciculus and the inferior longitudinal fasciculus of mTBI were measured in mTBI patients and controls at acute phase,subacute phase,5 weeks and 3 months post-trauma.The temporal changes of MRI data were observed.Results The FA values in the part of the white mat-ter fiber tracts reduced in the acute and subacute phase in mTBI patients (all P <0.05)in relative to controls (all P <0.05),At 5 weeks and 3 months post-trauma,the FA values also slightly lower in patients than controls.As for the genu of the corpus callosum and the splenium of the corpus callosum,the FA values in mTBI patients increased slightly at the acute stage (all P >0.05),but de-creased at 5 weeks-3 months post-trauma phase,though there was no significantly difference(all P >0.05).ADC values significantly decreased in the acute and subacute phase in mTBI patients,while they recovered thereafter (all P >0.05).Conclusion The sensi-tivity of DTI in detecting the lesions of mild traumatic brain damage is high,and it can display the damage of white matter.DTI could play an important role in the diagnosis of mTBI.

Objective To determine the expression of glial fibrillary acidic protein(GFAP) and vascular endothelial growth factor(VEGF) in the hippocampus of rats with Alzheimer's disease(AD), and to determine the effect of butylphthalide on them and its significance. Methods Sixty male adult rats were randomly divided into a model group, a Butylphthalide group, and a control group. AD models were established by injecting β-amyloid protein 1-42 into the hippocampus of rats. Sixty days later,the rats were sacrificed and both sides of the hippocampus were sectioned for immunohistochemistry. Results Positive cells of GFAP in the hippocampus of the model group increased and the expression of VEGF decreased statistically, compared with the control group(P<0.01). The positive cells of GFAP in the hippocampus of the butylphthalide group decreased and the expression of VEGF increased significantly, compared with the model group(P<0.05). Conclusion Butylphthalide may protect the neuron-vascular unit of the hippocampus of Alzheimer model rats by inhibiting the expression of GFAP and increasing the expression of VEGF.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.

The pathogenesis and etiology of still remain unknown. Current evidence suggests that the occurrence of depression may be related to a reduced secretion of neurotransmitters, neuronal apoptosis, inflammation, intestinal flora and other factors. Although the commonly used antidepressants such as SSRIs, SNRIs, NaSSA, and SARIs produce some therapeutic effects, they fail to relieve the full spectrum of the symptoms of depression. In recent years, esketamine was found to produce a potent and a long-lasting antidepressant effect by acting on the NMDA receptors. Herein the authors review the progress in the study of the pathogenesis and drug therapies of depression, the efficacy of esketamine treatment and the underlying mechanism, and the prospect of esketamine treatment. Currently the mechanism of the antidepressant effect of esketamine remains indeterminate and its clinical application is limited, but its effect in rapidly alleviating the symptoms of depression suggests its bright prospect for clinical applications.

OBJECTIVETo detect the expression of signal transducer and activator of transcription 3 (STAT3) and P-STAT3 in the brain of the APPswe/PS δE9 double transgenic mouse model of Alzhaimer's disease (AD) and investigate their possible role in AD.

METHODSAPPswe/PS δE9 double transgenic mice and control mice were examined for cerebral STAT3 and P-STAT3 expressions using immunothistochemistry.

RESULTSSTAT3 and P-STAT3 were expressed in the different regions of mouse brain. In the transgenic mice and the control mice, the positivity rates of STAT3 were 93.75% and 87.50% in the cerebral cortex, 87.50% and 43.75% in the basal forebrain, 81.25% and 37.50% in the hippocampus, and 62.50% and 0.00% in the cerebellum, respectively, showing significant differences between the mice in the STAT3 expressions in the basal forebrain, hippocampus and cerebellum (P<0.05). The positivity rates of P-STAT3 in the two groups were 0.00% and 0.00% in the cerebral cortex, 68.75% and 0.00% in the basal forebrain, 62.50% and 12.50% in the hippocampus, and 43.75% and 0.00% in the cerebellum, respectively, showing also significant differences in the basal forebrain, hippocampus and cerebellum (P<0.05). The expression of STAT3 was positively correlated with that of P-STAT3 in transgenic AD mice (P<0.05).

CONCLUSIONSTAT3 and P-STAT3 are highly expressed in the basal forebrain, hippocampus and cerebellum in transgenic AD mice and may participate in the pathological process of AD.

Alzheimer Disease ; metabolism ; Animals ; Cerebellum ; metabolism ; Cerebral Cortex ; metabolism ; Disease Models, Animal ; Hippocampus ; metabolism ; Mice ; Mice, Transgenic ; STAT3 Transcription Factor ; metabolism

OBJECTIVETo detect the expression of miRNA-135a-5p, miRNA-135a-2-3p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p in the brain tissue of the APPswe/PS δE9 double transgenic mouse model of Alzheimer's disease using real-time PCR.

METHODSSix-month-old APPswe/PS δE9 double transgenic mice and wild-type C57 mice of the same species were examined for the expressions of miRNA-135a-5p, miRNA-135a-2-3p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p in the brain tissue using real-time PCR.

RESULTSThe relative expression levels of the 5 miRNAs in the transgenic versus the wild-type mice were 0.73∓0.27 vs 1.08∓0.58, 2.47∓6.15 vs 1.65∓0.67, 0.72∓0.14 vs 1.31∓0.73, 0.57∓0.34 vs 1.06∓0.35, and 0.63∓0.26 vs 1.02∓0.18, respectively, showing significance differences in the expressions of miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p, and miR-669f-3p between the two groups (P<0.05).

CONCLUSIONSmiRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p are expressed differentially in APPswe/PS δE9 double transgenic mice, suggesting their important roles in the pathogenesis of Alzheimer disease.

Alzheimer Disease ; genetics ; metabolism ; Animals ; Brain ; metabolism ; Disease Models, Animal ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs ; genetics ; metabolism ; Real-Time Polymerase Chain Reaction ; methods

OBJECTIVETo observe the changes of miRNA expression profiles in APPswe/PSδE9 transgenic mice and explore the possible roles of miRNA in the pathogenesis of Alzheimer's disease.

METHODSUsing miRNA chip technique, we examined the miRNA expression in the brain tissue of 6-month-old APPswe/PSδE9 transgenic mice, with age-matched wild-type mice as the control group.

RESULTSTwelve miRNAs showed differential expressions by more than two folds in APPswe/PSδE9 transgenic mice, namely miRNA-135a, miRNA-135a-2*, miRNA-298, miRNA-466b-3p, miR-669-3p, miR-142-5p, miR-144, miR-466f-3p, miR-466g, miR-200a, miR-200b and miR-96. Five miRNAs were significantly down-regulated in the transgenic mice, including miRNA-135a, miRNA-135a-2*, miRNA-298, miRNA-466b-3p, and miR-669-3p.

CONCLUSIONThe 5 down- regulated miRNA may play important roles in the pathogenesis of AD in APPswe/PSδE9 transgenic mice.

Alzheimer Disease ; genetics ; metabolism ; Animals ; Disease Models, Animal ; Gene Expression Profiling ; Mice ; Mice, Transgenic ; MicroRNAs ; genetics ; metabolism ; Oligonucleotide Array Sequence Analysis ; Transcriptome