Effect of fingolimod on proliferation and migration of neural stem cells and astrocytes and its protective mechanism against spinal cord injury in mice / 吉林大学学报(医学版)

ABSTRACT

Objective; To investigate the effects of fingolimod (FTY720) on the migration and proliferation of neural stem cells (NSCs) and astrocytes of the mice, and to elucidate the protective effect of FTY720 on spinal cord injury (SCI) of the mice and its mechanism. Methods; The NSCs and astrocytes were cultured in vitro and divided into control group (treated with PBS) and experiment group (treated with 0. 1 μmol · L-1 FTY720). The SCI mice were divided into control group (given PBS by oral, n=10) and expriment group (given 1 mg · kg-1 · d-1 FTY720 by oral, n=10). The number of migration cells of NSCs and astrocytes in two groups was detected by Transwell experiment, and the number of migration cells and the number of proliferative neurospheres of NSCs were detected by immunofluorescence staining. The SCI void areas of the mice in two groups were detected by HE staining, and the dynamic recovery of motor function of the mice was assessed by Basso Mouse Scale (BMS) behavioral score. Results; The Transwell detection results showed that compared with control group, the number of migration cells of NSCs in expriment group was increased (P<0. 05), and the number of migration cells of astrocytes in expriment group was decreased (P<0. 05). The immunofluorescence detection results showed that compared with control group, the number of proliferative neurospheres of NSCs in expriment group was increased (P<0. 05), and the number of astrocytes in damaged SCI in expriment group was decreased (P<0. 05). The HE staining results showed that compared with control group, the SCI void area was decreased (P<0. 05). The BMS score results showed that the BMS score of the mice in expriment group was higher than that in control group (P<0. 05). Conclusion; FTY720 can promote the proliferation and migration of NSCs, inhibit the migration of astrocytes, decrease the formation of glial scar, and promote the motor function recovery of the mice after SCI.