Objective To establish a novel model of senile dementia in rats. Methods Fifty-two Wistar male rats were divided into 5 groups, group A was treated with a permanent bilateral occlusion of both carotid arteries (2-VO) first and then intraperitoneal injection of D-galactose (60 mg?kg -1 ?d -1 ,ip,42 d), group B with intraperitoneal injection of D-galactose (60 mg?kg -1 ?d -1 ,ip,42 d) first and then permanent bilateral occlusion of both carotid arteries, group C with 2-VO, group D with intraperitoneal injection of D-galactose, and group E (normal control) without the above treatment. All the rats were tested by using Morris water maze for their performance in learning and memory. Results Wistar rats treated with both 2-VO and D-galactose presented a significant diffe-rence from those simply treated by 2-VO and the normal rats. Conclusion The rat model of senile dementia induced by 2-VO and D-galactose simulated some characteristics of human senile dementia, and might be used in basic experiment study of senile dementia, such as vascular dementia, Alzheimer′s disease and mixed dementia.

In order to investigate the transfer and expression of Snail gene in human bone mesenchymal stem cells (MSCs) and to study effects of Snail gene modification on the CXCR4 expression of human MSCs and their capacity of migration to SDF-1 in vitro, the plasmid PCAGGSneo-Snail-HA or the control vector of PCAGGSneo was transferred into the cells. Fluorescence activated cell sorting analysis, immunofluorescence staining and RT-PCR were used to study the expression of CXCR4 by MSCs. Chemotaxis assays were performed to evaluate the migratory capacity of MSCs-Sna and MSCs-neo to SDF-1 in vitro. For the blocking assay, CXCR4 blocking antibody was added into cell culture. CXCR4 expression was higher in MSCs-Sna than that in MSCs-neo (P < 0.05). Chemotaxis assays showed that SDF-1alpha stimulated migratory activity of MSCs-Sna more than MSCs-neo in vitro (P < 0.05). Moreover, the SDF-1alpha-induced migratory activity of MSCs-Sna was inhibited in a concentration-dependent manner by a CXCR4-blocking antibody. It was concluded that Snail enhanced expression of CXCR4 in MSCs, providing a plausible mechanism for Snail-mediated MSCs transmigration to damaged tissues in vivo where SDF-1 has been shown to be up-regulated as part of injury responses.
Bone Marrow Cells ; cytology ; Cell Movement ; genetics ; Cells, Cultured ; Chemokine CXCL12 ; metabolism ; Humans ; Mesenchymal Stromal Cells ; cytology ; metabolism ; Receptors, CXCR4 ; genetics ; metabolism ; Snail Family Transcription Factors ; Transcription Factors ; genetics ; Transduction, Genetic