| Objective:To observe the histologic changes and the expression of myelin basic protein (MBP) by immunohitochemistry, we use the repeated focal cerebral ischemia and reperfusion model to cause the cerebral white matter damage after ischemic rats were treated with methylcobalamin and to discuss the neuroprective mechanism and the therapic effect of methylcobalamin from cell and molecular levels.Methods:Male Wistar rats (n=45) were divided into sham-operation groups(n=15), cerebral ischemia and reperfusion groups (n=15) and therapic groups with methylcobalamin (n=15) at random . Every group was divided into 1w, 2w and 4w group by reperfusion time. Cerebral ischemic modles were made by clamping bilateral carotid arteries for 15min then reperfuse 60min. Subsequently clamp for 15min then reperfuse for 1w, 2w and 4w. Every rat was killed at the specific time points to take brains. Sections were stained with HE for histologic changes and immunohistochemistry for MBP expression .The data were analysised by SAS6.12 software. Intra-animal comparisons were done using paired t-test , ANOVA and student-Newman-Keuls test in analysis-reason-design data, while comparisons between groups were done using q-test and ANOVA and student-Newman-Keuls test in analysis-reason-design data. Results:We observed the pyramidal neurons in hippocampus CA1 in ischmia and reperfusion groups in which express long trail, pyknosis, karyorrhexis and karyolysis. The normal and abnormal pyramidal neurons in the therapic groups were observed meanwhile the normal neurons were more than the abnormal ones. The changes were more obvious in 2w and 4w.The Comparised the ischemia and reperfusion groups with the sham-operation groups, MBP expression in corpus callosum ,subventricle and internal capsule in 1w was no difference, but they increased much more in 2w and 4w(p<0.05), especially the most apparent in 2w(p<0.001). Comparising the therapic groups with the ischemia and reperfusion ones, the MBP expression was no difference, but they decreased apparently in 2w and 4w(P<0.05). Comparising therapic groups with sham-operation groups ,MBP expression was no difference. In the ischemic and reperfusion groups, MBP expression reached the most high point(P<0.05)and backed to the level in 1w. In internal capsule, MBP expression was difference in 2w and 4w comparised with the ones in 1w respectively(P<0.05).Both in the ischemic and reperfusion groups and the sham-operation groups MBP expression was no difference in 3 time points. Discuss:The cerebral white matter damage were very often seen in clinical practice and related with the selective and vulnerable to ischemic damage .The nonreversible damage in cerebral white matter destroy the message transmission then affect seriously the global function of CNS. The cerebral white matter lesion were related with cognitive impairment and was an important prognostic factor for stroke and cognitive impairment. So it is part of role to study the cerebral white matter ischemia lesion in LA. OLG is the forming cells of myelin in CNS, which can synthesis the components of myelin, phospholipid and MBP.OLG is more sensitive than neurons even in specific brain when subjected with ischemic and anoxic damage. The serious ischemic damage of OL make the gene expression related with myelin phospholipid inhibit. Although the cell was survival, the synthesis of myelin phospholipid was also decreased. Because its resolvement and destroyed were taken long half life,2.5-8.7 days, myelin necrosis or demyelination degeneration often observed in 10-14 days after ischemia. Myelination requires an extraordinary capacity for synthesize membranes at a given time. Only after OLG split into myelin forming cells totally, MBP mRNA begin posttranslational modifications. Posttranslational modifications include NH2-terminal acetylation, phosphorylation, and methylation. The methlation of MBP may be the most important for compaction of the myelin membrane. Recently studies on methlination suggest, the methlation of the 107 A...
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