α-生育酚对颅脑创伤大鼠神经功能的保护作用研究

发布时间：2018-06-15 14:18

本文选题：α-生育酚 + TBI　；参考：《天津医科大学》2017年硕士论文

【摘要】：目的:通过研究α-生育酚对TBI大鼠神经及脑组织的保护来评价其对TBI的治疗效果。方法:选取160只雄性成年SD大鼠,随机分为假手术组、TBI组、常规性治疗组及TBI常规治疗+α-生育酚治疗组,每组各40只。假手术组仅切开头皮及磨骨窗,不进行打击,其余各组采用可控性电子皮质打击仪建立模型。常规性治疗组建模后给予抗感染等治疗,治疗时间为7 d,TBI常规治疗+α-生育酚治疗组在常规性治疗组基础上于TBI后6h腹腔注射α-生育酚200 mg/kg,连续注射7 d,每12h给药1次,假手术组、TBI组于相同时间注射生理盐水。分别于TBI后12 h、24 h、3 d、7 d对各组大鼠进行平衡木行走实验、水迷宫实验以测定大鼠神经功能。依据m NSS评分对实验组及对照组大鼠术后相应时间点神经功能进行评分。利用ELISA法测定各组大鼠外周血不同时间点一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)、催化单胺氧化脱氨反应酶(MAO)等抗氧化物水平,然后处死大鼠取其脑组织,进行HE染色检测病理改变,应用免疫组织化学法测定大鼠脑组织中Bax、Bcl-2蛋白表达情况。结果:(1)水迷宫实验中TBI常规治疗+α-生育酚治疗组治疗在TBI后12 h、24h、3 d、7 d到达平台时间显著短于TBI组及常规性治疗组(P0.05),而常规性治疗组治疗12 h、24 h、3 d、7 d到达平台时间显著短于TBI组(P0.05)。(2)平衡木行走实验中TBI常规治疗+α-生育酚治疗组在TBI后12 h、24 h、3 d、7 d到达平台时间显著短于TBI组及常规性治疗组(P0.05),而常规性治疗组在TBI后12 h、24 h、3 d、7 d到达平台时间显著短于TBI组(P0.05)。(3)TBI常规治疗+α-生育酚治疗组在TBI后12 h、24 h、3 d、7 dm NSS评分均低于TBI组及常规性治疗组(P0.05),而常规性治疗组治疗12 h、24 h、3 d、7 d m NSS评分均低于TBI组(P0.05)。(4)通过脑组织病理切片可观察到TBI常规治疗+α-生育酚治疗组组织程度较TBI组及常规性治疗组轻,而常规性治疗组脑组织受损程度较TBI组轻。(5)经干、湿重法测定可知,TBI常规治疗+α-生育酚治疗组大鼠脑组织水肿程度较TBI组及常规性治疗组轻(P0.05),而常规性治疗组脑组织水肿程度较TBI组轻(P0.05)。(6)TBI常规治疗+α-生育酚治疗组在TBI后12 h、24 h、3 d、7 d血清NO、SOD水平显著高于TBI组及常规性治疗组(P0.05),而治疗12 h、24 h、3 d、7 d血清MDA、MAO低于TBI组及常规性治疗组(P0.05)。常规性治疗组治疗12 h、24 h、3 d、7 d血清NO、SOD水平显著高于TBI组(P0.05),而治疗12 h、24 h、3 d、7 d血清MDA、MAO低于TBI组(P0.05)。(7)TBI常规治疗+α-生育酚治疗组Bax阳性细胞数较常规性治疗组显著下降,Bcl-2阳性细胞较常规性治疗组显著升高(P0.05)。结论:(1)α-生育酚能在很大程度上减轻TBI大鼠神经细胞受损程度,显著改善大鼠TBI后神经功能;(2)α-生育酚可通过调节过氧化物生成而减轻机体过氧化反应对脑组织的损伤;(3)α-生育酚可通过减轻脑水肿而发挥保护脑组织的作用;(4)α-生育酚可通过抑制Bax蛋白表达和促进Bcl-2蛋白表达来减少TBI后神经细胞凋亡来发挥脑组织保护作用。
[Abstract]:Objective: To evaluate the protective effect of alpha tocopherol on the nerve and brain tissue of TBI rats to evaluate its effect on TBI. Methods: 160 adult male adult SD rats were randomly divided into sham operation group, group TBI, routine treatment group and TBI routine therapy + alpha tocopherol treatment group with 40 rats in each group. The sham operation group was only cut into the scalp and the grinding window. The other groups were modeled by controllable cortico percussion instrument. The treatment time was 7 d after routine treatment. The TBI routine treatment + alpha tocopherol group was injected with alpha tocopherol 200 mg/ kg after TBI and 7 d, 1 times per 12h, sham operation group, TB. The I group was injected with normal saline at the same time. After TBI 12 h, 24 h, 3 D and 7 d, the rats were carried out the balance Wood Walking experiment and the water maze test was used to determine the nerve function of the rats. According to the m NSS score, the nerve function of the experimental group and the control group was evaluated at corresponding time points after operation. The peripheral blood of each group was measured by ELISA method. The levels of nitric oxide (NO), superoxide dismutase (SOD), malondialdehyde (MDA), catalyzed mono amine oxidation deamination enzyme (MAO) and other antioxidants, were then executed to obtain their brain tissue, HE staining was used to detect pathological changes. The expression of Bax and Bcl-2 in the brain tissue of rats was detected by immunohistochemistry. Results: (1) water maze experiment (1) TBI routine treatment + alpha tocopherol treatment group was treated at 12 h after TBI, 24h, 3 D, 7 d to reach the platform time significantly shorter than the TBI group and the conventional treatment group (P0.05), while the conventional treatment group was 12 h, 24 h, 3 D, and 7 d reached the platform time significantly shorter than that of the group. (2) the routine treatment + alpha tocopherol treatment group was 12, The arrival time of 24 h, 3 D, 7 d was significantly shorter than that of the TBI group and the routine treatment group (P0.05), while the conventional treatment group was 12 h, 24 h, 3 D, 7 d, significantly shorter than the TBI group (P0.05). (3) the routine treatment + alpha tocopherol treatment group was 12, 24 and 3. In the treatment group, 12 h, 24 h, 3 D, 7 d m NSS scores were lower than those in the TBI group (P0.05). (4) the histological section of the brain tissue was observed to be lighter than the TBI group and the conventional treatment group, while the normal treatment group was lighter than the TBI group. (5) the routine treatment of TBI with the dry, wet weight method showed that the normal treatment group was treated with the routine treatment. The edema degree of brain tissue in the group of alpha tocopherol was lighter than that of the TBI group and the conventional treatment group (P0.05), while the degree of edema in the brain tissue was lighter in the routine treatment group than in the TBI group (P0.05). (6) the routine TBI therapy + alpha tocopherol treatment group was 12 h, 24 h, 3 D, 7 d serum NO, and the SOD water level was significantly higher than that in the group and the routine treatment group, while the treatment was 12, 24, 24. 24 H, 3 D, 7 d serum MDA, MAO lower than TBI group and routine treatment group (P0.05). The routine treatment group was treated with 12 h, 24 h, 3 D, 7 d serum NO. Bcl-2 positive cells were significantly higher than those in the conventional treatment group (P0.05). Conclusion: (1) alpha tocopherol can reduce the degree of nerve cell damage in TBI rats to a great extent and significantly improve the neurologic function of rats after TBI; (2) alpha tocopherol can reduce the injury of peroxidation to brain tissue by regulating the formation of peroxides; (3) alpha tocopherol can be used. (4) alpha tocopherol can protect the brain tissue by inhibiting the expression of Bax protein and promoting the expression of Bcl-2 protein to reduce the apoptosis of neurons after TBI.
【学位授予单位】：天津医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R651.15

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