| Objective:Foxp3 transcription factor plays a key function in the transfer process in the central nervous system. The related substances of Foxp3 transcription factor not only can be combined with other types of nerve neurotransmitter involved brain and central nervous system neurotransmitter effect, in addition, Foxp3 transcription factor plays a critical function in all aspects like activity, mood changes in the human body even body’s appetite regulation. In short, whether it is the synthesis of Foxp3 transcription factors, or the release /uptake of substances in the body, or the other abnormal aspects will show abnormal neurological symptoms.During the last ten years, the relationship between the content of regulatory T cells and tumor, body nerve traumatic diseases and autoimmune diseases is more and more deeply. Especially the relationship between content changes of CD4+CD25+ regulatory T cells and transcription factor Foxp3 and related diseases has become a hot and difficult issue of research in recent years. Study on the relationship between the content of the system related to nerve damage and CD4+CD25+ regulatory T cells and transcription factor Foxp3 is not a lot, especially the basic research on animal experiment is less, after nerve injury, the mechanism and process of content changes and the incidence of CD4+CD25+ regulatory T cells and transcription factor Foxp3 in animal serum is still not very clear.To determine the correlation between the NSS scores and the levels of the CD4+CD25+ regulatory T cells and Foxp3 contents between the brain injured and normal rats, a study was conducted by measuring several parameters such as the NSS rates, the frequencies of CD4+CD25+ T cells in peripheral blood and the contents of transcription factor Foxp3 in the brain tissue by using a rat model of brain damage,and analyzing the effect of brain damage progression imposed on these parameters,and eventually establishing the correlation between them. This study will provide the scientific support for the future treatments of symptoms caused by the cranial nerve damages.Methods:1 Experimental methods: The experiment was divided into two groups, 20 rats in each group. During experiment 1, 3, 7, 14 days were sacrificed 5 rats in each group. According to the modified method of Zea-Longer line technology, the rat brain damage model was made,using hypodesis to establish the right middle cerebral artery ischemia, and eventually induced the brain damage. The correlation of the brain damage with the frequencies of CD4+ CD25+ regulatory T cells(test by flow cytometry)and the contents of Foxp3 in brain tissue(test with immunohistochemistry)was studied by comparing NSS scores and relative parameters between control rats and test rats.2 Statistical methods: All data were analysed by SPSS18.0 software. Fisher and χ2 test were used for analyzing countable data. The means were analysed by ANOVA. The relationship between the brain damage and the NSS scores, the frequencies of CD4+ CD25+ regulatory T cells and the level of Foxp3 in brain tissue were analysed by Sperman rank correlation analysis and multiple stepwise regression. The difference had statistical significance if P<0.05.Results:1 In the test groups, sign of white brain infarction was appeared in the damaged side’s Basal ganglia and cortex of the rats while in the control groups the sign was not appeared, which proved the animal model was made successfully.2 At the same time point, the difference of the NSS between the test group and control group rats had statistical significance(P<0.05) and at different time points, the difference of the NSS in the test group rats had statistical significance(P<0.05).3 The NSS scores of test group were higher than those of the control group and the two factors of rats grouping and the persistent times of cerebral nerve damage showed a significant interaction effect(P<0.05).4 On the first day and third day after the brain damage, the mean frequency of CD4+CD25+ regulatory T cells in peripheral blood of test group rats had no significant difference with that of the control group rats, but it was higher than that of control group rats(P<0.05)on the seventh day and the fourteenth day after the brain damage.5 The mean frequencies of CD4+CD25+ regulatory T cells in peripheral blood of test group rats,measured at different time points,had significant difference(P<0.05),while it was on the contrary in the control group rats(P>0.05). Further analysis indicated that there was an interaction effect between the frequencies of CD4+CD25+ regulatory T cells in test group rats and the persistent times of brain damage.6 In the test group, the cerebral infarction had been found in the rats brain tissue, the brain nerve damaged region showed typical ischemic pathological change and the boundary between normal brain tissue and tissue around the lesion was very clear. Further observation showed that in the necrosis range of cranial nerve damaged part, a number of brain nerve cells were necrotic in different degrees because of ischemia, the construction of the brain nerve cells had disappeared, it was difficult to identify the neuronal shape of the brain nerve, the number of nerve cells in damaged brain appeared reduction in different degrees and the cytoplasm of the brain nerve cells showed vacuolar degeneration.7 On the first day, third day, seventh day and fourteenth day after the animal model had been successfully prepared, considerable quantities of Foxp3 were detected in local damaged sites, while the Foxp3 contents at normal brain tissue of control group rats were low.8 On the first day, third day, seventh day and fourteenth day after the animal model had been successfully prepared, there was a negative correlation between the NSS score and the frequencies of CD4+CD25+ regulatory T cells in the peripheral blood of the test group rats(P<0.05).9 Concerning the contents of CD4+ and CD25+regulatory T cells in the blood and the Foxp3 expressed in the brain tissue and other subjects as the independent variable, and the NSS total scores as dependent variable, we use multiple stepwise regression to analysis. The results showed that:CD4+ and CD25+ regulation T cells and Foxp3 count into the regression equation, suggesting that CD4+ and CD25+ regulation T cells and Foxp3 expressed in brain tissue have a greater impact on rats with NSS score.Conclusions:1 If the rat’s brain nerve is damaged, the content of CD4+CD25+ regulatory T cells in the blood at different times after it is damaged will show dynamic changes, which tell us that CD4+CD25+ regulatory T cells participate in the occurrence and development process of pathophysiology after the rat brain damaged.2 The content of Foxp3 in rat brain nerve damaged sites has a close relationship to the injuried formation of cranial nerve and Foxp3 is mainly expressed in the damaged lesion and the areas which are surrounding it.3 After the rat brain nerve is damaged, neuronal cell bodies of local brain tissue can appear narrow, deep dyeing and nucleus pyknosis and the nerve cells appear a large number of necrosis phenomenon, with a number of pathological changes such as most of the cell structures disappear, neuron shape is not easy to identify, cytoplasmic shows vacuolar degeneration and impaired foci appears a large number of glial cell proliferation.4 The relationship between the expression of CD4+CD25+ regulatory T cells in the blood after rat brain nerve is damaged and the degree of nerve function damaged is a negative correlation, which indicates that CD4+CD25+ regulatory T cells in immune regulation after acute cerebral ischemia might play a protective role. |
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