AIM To compare the effects of intravenous route and peritoneal route on liver targeted uptake andexpression of plasmid delivered by glyco-poly-L-lysine (G-PLL).METHODS The plasmid pTM/MMP-1 which could be expressed in eukaryotic cells was bound to thegalactose-terminal glyco-poly-L-lysine (G-PLL), and then was transferred into Wistar rats by intravenousand intraperitoneal injection respectively. Afterwards the expression and distribution of the plasmid wereobserved at different time points by in situ hybridization and immunohistochemistry.RESULTS The plasmid could be expressed obviously in 24 hours after being transferred in vivo by bothintravenous and intraperitoneal route. One week later the expression began to decrease, and still could beovserved three weeks later. Although both the intravenous and intraperitoneal route could deliver theplasmid to liver targetly, the effect of the former was better as compared with that of the latter.CONCLUSION Intravenous route was better for liver targeted uptake and expression of G-PLL-boundplasmid than peritoneal route.

To date, it remains poorly understood whether astrocytes can be easily reprogrammed into neurons. Mash1 and Brn2 have been previously shown to cooperate to reprogram fibroblasts into neurons. In this study, we examined astrocytes from 2-month-old Sprague-Dawley rats, and found that Brn2 was expressed, but Mash1 was not detectable. Thus, we hypothesized that Mash1 alone could be used to reprogram astrocytes into neurons. We transfected a recombinant MSCV-MASH1 plasmid into astrocytes for 72 hours, and saw that all cells expressed Mash1. One week later, we observed the changes in morphology of astrocytes, which showed typical neuro-nal characteristics. Moreover,β-tubulin expression levels were signiifcantly higher in astrocytes expressing Mash1 than in control cells. These results indicate that Mash1 alone can reprogram astrocytes into neurons.

There are several major pathological changes in Alzheimer’s disease, including apoptosis of cho-linergic neurons, overactivity or overexpression ofβ-site amyloid precursor protein cleaving enzyme 1 (BACE1) and inflammation. In this study, we synthesized a 19-nt oligonucleotide targeting BACE1, the key enzyme in amyloid beta protein (Aβ) production, and introduced it into the pSilenCircle vector to construct a short hairpin (shRNA) expression plasmid against the BACE1 gene. We transfected this vector into C17.2 neural stem cells and primary neural stem cells, resulting in downregulation of the BACE1 gene, which in turn induced a considerable reduction in reducing Aβprotein production. We anticipate that this technique combining celltransplantation and gene ther-apy wil open up novel therapeutic avenues for Alzheimer’s disease, particularly because it can be used to simultaneously target several pathogenetic changes in the disease.