本文選題：α-生育酚 + TBI��； 參考：《天津醫(yī)科大學》2017年碩士論文

【摘要】：目的:通過研究α-生育酚對TBI大鼠神經(jīng)及腦組織的保護來評價其對TBI的治療效果。方法:選取160只雄性成年SD大鼠,隨機分為假手術組、TBI組、常規(guī)性治療組及TBI常規(guī)治療+α-生育酚治療組,每組各40只。假手術組僅切開頭皮及磨骨窗,不進行打擊,其余各組采用可控性電子皮質(zhì)打擊儀建立模型。常規(guī)性治療組建模后給予抗感染等治療,治療時間為7 d,TBI常規(guī)治療+α-生育酚治療組在常規(guī)性治療組基礎上于TBI后6h腹腔注射α-生育酚200 mg/kg,連續(xù)注射7 d,每12h給藥1次,假手術組、TBI組于相同時間注射生理鹽水。分別于TBI后12 h、24 h、3 d、7 d對各組大鼠進行平衡木行走實驗、水迷宮實驗以測定大鼠神經(jīng)功能。依據(jù)m NSS評分對實驗組及對照組大鼠術后相應時間點神經(jīng)功能進行評分。利用ELISA法測定各組大鼠外周血不同時間點一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)、催化單胺氧化脫氨反應酶(MAO)等抗氧化物水平,然后處死大鼠取其腦組織,進行HE染色檢測病理改變,應用免疫組織化學法測定大鼠腦組織中Bax、Bcl-2蛋白表達情況。結果:(1)水迷宮實驗中TBI常規(guī)治療+α-生育酚治療組治療在TBI后12 h、24h、3 d、7 d到達平臺時間顯著短于TBI組及常規(guī)性治療組(P0.05),而常規(guī)性治療組治療12 h、24 h、3 d、7 d到達平臺時間顯著短于TBI組(P0.05)。(2)平衡木行走實驗中TBI常規(guī)治療+α-生育酚治療組在TBI后12 h、24 h、3 d、7 d到達平臺時間顯著短于TBI組及常規(guī)性治療組(P0.05),而常規(guī)性治療組在TBI后12 h、24 h、3 d、7 d到達平臺時間顯著短于TBI組(P0.05)。(3)TBI常規(guī)治療+α-生育酚治療組在TBI后12 h、24 h、3 d、7 dm NSS評分均低于TBI組及常規(guī)性治療組(P0.05),而常規(guī)性治療組治療12 h、24 h、3 d、7 d m NSS評分均低于TBI組(P0.05)。(4)通過腦組織病理切片可觀察到TBI常規(guī)治療+α-生育酚治療組組織程度較TBI組及常規(guī)性治療組輕,而常規(guī)性治療組腦組織受損程度較TBI組輕。(5)經(jīng)干、濕重法測定可知,TBI常規(guī)治療+α-生育酚治療組大鼠腦組織水腫程度較TBI組及常規(guī)性治療組輕(P0.05),而常規(guī)性治療組腦組織水腫程度較TBI組輕(P0.05)。(6)TBI常規(guī)治療+α-生育酚治療組在TBI后12 h、24 h、3 d、7 d血清NO、SOD水平顯著高于TBI組及常規(guī)性治療組(P0.05),而治療12 h、24 h、3 d、7 d血清MDA、MAO低于TBI組及常規(guī)性治療組(P0.05)。常規(guī)性治療組治療12 h、24 h、3 d、7 d血清NO、SOD水平顯著高于TBI組(P0.05),而治療12 h、24 h、3 d、7 d血清MDA、MAO低于TBI組(P0.05)。(7)TBI常規(guī)治療+α-生育酚治療組Bax陽性細胞數(shù)較常規(guī)性治療組顯著下降,Bcl-2陽性細胞較常規(guī)性治療組顯著升高(P0.05)。結論:(1)α-生育酚能在很大程度上減輕TBI大鼠神經(jīng)細胞受損程度,顯著改善大鼠TBI后神經(jīng)功能;(2)α-生育酚可通過調(diào)節(jié)過氧化物生成而減輕機體過氧化反應對腦組織的損傷;(3)α-生育酚可通過減輕腦水腫而發(fā)揮保護腦組織的作用;(4)α-生育酚可通過抑制Bax蛋白表達和促進Bcl-2蛋白表達來減少TBI后神經(jīng)細胞凋亡來發(fā)揮腦組織保護作用。
[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.
【學位授予單位】：天津醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R651.15

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本文編號：2022335