| NSCs are capable of proliferating and can give rise to mature descendants of different types of cells both in vitro and in vivo. Discovery of this kind of cells opens vistas for cell therapy of various pathological processes in the CNS, from metabolic and genetic neurodegenerative disorders to posttraumatic diseases. To make the transplanted cells functionally and efficiently integrate into the host nervous network, the high viability and correct differentiation of the donor cells must be obtained. Thus the objective of this study is to find some ways to improve the efficiency of cell therapy, that is. to optimize the microenvironment of NSCs and in turn prompt them to functinally repair abnormal CNS.In the first part, optimization of X-gal staining method, which is correlated with pH, incubating time, perfusion and some other parameters, was successfully got and used in the subsequent experiment, viz, comparing the behaviours of primary NSCs and immortal NSC line after transplantation. Primary cultured NSCs (labbled by Hoechst33342) and C17.2(a kind of immortal NSC cell line expressing B-galactosidase) were injected into thelateral ventricles of neonatal mouse, then the cells' survial,integration and migration were compared 1W and 6W after the transplantation. The results are as follows:After lw,the living cells of primary NSCs were much more than C17.2 (P<0.01) ,besides,the former mainly resided in the ventricle whereas the latter integrated to the parenchyma. As to C17.2, the proportion of mitotic cells was very high and up to 69.4 ?2.2%. After 6w, the total number of C17.2 increased greatly while the primary NSCs decereased,they had no significant difference .At this time,most primary NSCs also integrated to the parenchyma,the migrating diatance of C17.2 is larger than primary NSCs (P<0.05) . Besides, the proportion of mitotic cells decreased to 9.4 ?1.2% and the cells bearing processes reached to 89.8?13.4%. These results indicate that comparing to primary NSCs, C17.2 can't survive well in cerebrospinal fluid,but they will proliferate and migrate better once they integrate into the parenchyma.In the second part of this study, the effects of inosine on C17.2 in vitro were detected. The results show that inosine can prompt proliferation of C17.2 at the range of 0~800 n M and process outgrowth 50-800 M M, also 100 u M inosine can improve the expression level of p-tubulin III, while at 1000 P M,such effects were reversed. In this part the direct neurotrophic effects of inosine were explored. MTT value, morphological characteristics under light and electron microscopy, DNA gel electrophresis results, and Hoechst33342 dying results show that inosine can protect NSCs against apoptosis induced by HiOi significantly in a dose dependent manner.In the last part of the study, the primary detection of OECs' effects on C17.2 was made. The results indicate that there exists a positive cooperativeeffect between OECs and C17.2 in proliferation (P<0.05) ; OECs can't influence the differentiation of C17.2; OECs showed more permissiveness comparing to 3T3. OECs and C17.2 can contact closely or even overlap each other, under such circumstance, C17.2 usually spread more and longer processes. Sometimes, their processes prolonged parallel with OECs'. This maybe because such cells can express higher level of adhesion molecular, such as LI, etc.
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