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Objective To observe the effects of electro-acupuncture on the expression and inhibition of DNA binding protein 2 (Id2) and myelin basic protein (MBP),and to explore the mechanism of remyelinization after compressive spinal cord injury (CSCI) in rats.Methods Fifty-four SD rats were randomly divided into a control group and a treatment group,and each was further subdivided into 3 time point subgroups:3,7 and 14 days.There were 9 rats in each subgroup.The CSCI models were made with a self-designed method.The acupuncture points Jiaji (EX-B2),bilateral Zusanli (ST36) and Taixi (KI3) were selected for treatment.Electro-acupuncture (continuous wave,2 Hz,1.5 V)was applied to the bilateral Zusanli (ST36) and Taixi (KI3) points.The control group received the injury but no treatment.The changes in the ultrastucture of the nerve fibers＇ white matter were de-termined by transmission electron microscopy (TEM).The alterations in the expression of MBP and Id2 were observed by double labeled immunofluorescence and Western blotting on the 3rd,7th and 14th day after the injury.Results TEM showed that the myelin sheaths in the control group had degenerated,swollen,and even broken down after CSCI.Changes to the myelin sheaths in the treatment group were milder than those in the control group.The immunofluorescence results showed the amount of Id2-immunoreactive oligodendrocytes in the control group to be (20 ±2) on the 3rd day after CSCI,becoming (16 ± 1) on the 14th day.The differences among the 3 control subgroups were not statistically significant.The amount of Id2-immunoreactive oligodendrocytes in the treatment group was (13 ± 1) on the 3rd day,reaching a minimum the 14th day.The differences among the 3 treatment groups were statistically significant.The differences compared with the control group at the same time points were also statistically significant.Western blotting showed that the expression of Id2 in the contrast and treatment groups was (1.12 ±0.12) and (0.67 ±0.01) respectively on the 3rd day after CSCI,and both decreased with time.The expression of Id2 in both groups reached their minima ((0.86 ±0.02) and (0.25 ±0.01) respectively) on the 14th day.The difference between the treatment groups and the contrast group was statistically significant at each time point.The expression of MBP in the contrast and treatment groups at day 3 was (0.44 ± 0.02) and (0.67 ± 0.04) respectively,and these increased with time.The expression of MBP in both groups peaked at the 14th day (at (0.95 ± 0.04) and (1.74 ± 0.09) respectively).These differences were again statistically significant.Conclusion Electro-acupuncture can regulate the expression of Id2 and MBP after CSCI.The down-regulation of Id2 which controls MBP negatively and the up-regulation of MBP may contribute to remyelination in the injured spinal cord.
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@#Objective To observe the effect of Ginkgolide B of various consistency on the differentiation of neuron stem cells (NSCs).MethodsNSCs were cultured in differentiation medium containing Ginkgolide B of various consistency for 3 and 7 days, the neurites length and cell body area were measured by inverted phase-contrast micrograph, then neurofilament-200 (NF-200), glial fibrillary acidic protein (GFAP), adenomatus polyposis coli (CC-1) expression were detected and counted by fluorescence microscope. The suppressor of cytokine signaling-2 (SOCS2), inhibitor of DNA binding-2 (Id2) were alsoimmunostained. The percentage of positive cells were counted respectively.ResultsThe neurites length and cell body area in Ginkgolide B groups were obviously larger than that in the control group. The percentage of NF, GFAP positive cells in Ginkgolide B groups increased with dosage increasing of Ginkgolide B. Compared with the normal control group, the percentage of SOCS2 positive cells increased significantly ( P<0.01) and the percentage of Id2 positive cells decreased significantly ( P<0.01) in Ginkgolide B groups.ConclusionGinkgolide B can promote NSCs to differentiate into neuron and astrocyte, the percentage of astrocyte is increased with a dosage-dependent relationship with Ginkgolide B.