本文選題：視神經(jīng)損傷 + 地塞米松�。� 參考：《新疆醫(yī)科大學(xué)》2012年碩士論文

【摘要】：目的：探討急性視神經(jīng)損傷后經(jīng)翼點(diǎn)入路視神經(jīng)管減壓術(shù)以及應(yīng)用地塞米松藥物治療對(duì)兔視網(wǎng)膜神經(jīng)節(jié)細(xì)胞（RGC）的凋亡過程干預(yù)作用及兩種處理方案對(duì)視網(wǎng)膜神經(jīng)節(jié)細(xì)胞中腫瘤壞死因子免疫活性的影響。方法：96只新西蘭兔均建立右眼外傷性視神經(jīng)損傷模型，左眼作為空白對(duì)照。所有動(dòng)物模型按完全隨機(jī)方法分為手術(shù)組，地塞米松組，損傷組，每組24只。按損傷后3、7、14、21天4個(gè)時(shí)間點(diǎn)，每組又分為4個(gè)小組，每小組8只。手術(shù)小組在急性視神經(jīng)損傷模型建立后24h-48h間全麻下施行經(jīng)翼點(diǎn)入路視神經(jīng)管減壓術(shù)；地塞米松小組在視神經(jīng)損傷模型建立后持續(xù)給予地塞米松（1mg/kg，一日一次）。于損傷后第3、7、14、21天分別按隨機(jī)原則處死相應(yīng)天數(shù)手術(shù)小組、地塞米松小組，損傷小組動(dòng)物模型，取材后分別行視網(wǎng)膜組織HE染色和TUNEL染色，光鏡下對(duì)各小組視網(wǎng)膜神經(jīng)節(jié)細(xì)胞進(jìn)行計(jì)數(shù)并采用酶聯(lián)免疫吸附試驗(yàn)（ELISA）檢測(cè)TNF-濃度。結(jié)果：（1）隨損傷后時(shí)間延長，損傷小組視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)逐漸減少，且在各時(shí)間點(diǎn)存活視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)存在差異并具有統(tǒng)計(jì)學(xué)意義；在各時(shí)間點(diǎn)手術(shù)小組與損傷小組的存活視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)存在差異并具有統(tǒng)計(jì)學(xué)意義；各時(shí)間點(diǎn)地塞米松小組與損傷小組的存活視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)存在差異并具有統(tǒng)計(jì)學(xué)意義。（2）手術(shù)小組在早期（3d、7d）的存活視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)明顯高于地塞米松小組，差異具有統(tǒng)計(jì)學(xué)意義；手術(shù)小組在中晚期（14d、21d）的存活視網(wǎng)膜神經(jīng)節(jié)細(xì)胞數(shù)略高于地塞米松小組，差異無統(tǒng)計(jì)學(xué)意義。（3）在不同的時(shí)間點(diǎn)手術(shù)小組TNF-α濃度均明顯低于損傷小組并具有統(tǒng)計(jì)學(xué)意義；不同的時(shí)間點(diǎn)地塞米松小組TNF-α濃度均明顯低于損傷小組并具有統(tǒng)計(jì)學(xué)意義。（4）在早中期（3d、7d、14d）時(shí)間點(diǎn)手術(shù)小組TNF-α濃度均明顯低于地塞米松小組并具有統(tǒng)計(jì)學(xué)意義；但在晚期（21d）手術(shù)小組與地塞米松小組兩組無明顯差異，，無統(tǒng)計(jì)學(xué)意義。結(jié)論：急性視神經(jīng)損傷后RGC凋亡是一個(gè)持續(xù)的細(xì)胞凋亡過程。經(jīng)翼點(diǎn)入路視神經(jīng)管減壓術(shù)治療對(duì)急性視神經(jīng)損傷后RGC具有保護(hù)作用。視神經(jīng)損傷后持續(xù)應(yīng)用地塞米松對(duì)RGC具有保護(hù)作用。經(jīng)翼點(diǎn)入路視神經(jīng)管減壓術(shù)治療和應(yīng)用地塞米松可減輕急性視神經(jīng)損傷后TNF-α濃度的急性升高。
[Abstract]:Objective: to investigate the effect of decompression of optic canal via pterygoid approach and dexamethasone drug therapy on apoptosis of retinal ganglion cells in rabbits after acute optic nerve injury. Effect of tumor necrosis factor on immune activity in ganglion cells. Methods the traumatic optic nerve injury model of right eye was established in 96 New Zealand rabbits, and the left eye was used as blank control. All animal models were randomly divided into operation group, dexamethasone group and injury group with 24 rats in each group. Each group was divided into 4 groups with 8 rats in each group. After the establishment of the model of acute optic nerve injury, the operative group underwent tranpterional approach optic canal decompression under general anesthesia between 24h-48h, and the dexamethasone group was continuously given dexamethasone 1 mg / kg once a day after the establishment of the optic nerve injury model. On the 21st day after injury, the corresponding days of operation group, dexamethasone group and injury group were sacrificed according to random principle. The retinal tissues were stained with HE and TUNEL respectively. Retinal ganglion cells were counted under light microscope and TNF- concentration was detected by Elisa. Results the number of retinal ganglion cells in the injured group decreased gradually with the extension of the time after injury, and the number of retinal ganglion cells survived at each time point was different and had statistical significance. There were significant differences in the number of viable retinal ganglion cells between the operative group and the injured group at each time point. The number of viable retinal ganglion cells in the dexamethasone group and the injured group was significantly higher than that in the dexamethasone group. The number of viable retinal ganglion cells in the surgical group was slightly higher than that in the dexamethasone group. There was no significant difference in TNF- 偽 concentration between the two groups at different time points, and the TNF- 偽 concentration was significantly lower in the operation group than in the injury group. The concentration of TNF- 偽 in the dexamethasone group was significantly lower than that in the injury group at different time points (P < 0.05). The concentration of TNF- 偽 in the operation group was significantly lower than that in the dexamethasone group at the early and middle stage. However, there was no significant difference between the operative group and dexamethasone group at the late stage of 21 d. Conclusion: RGC apoptosis is a continuous process of apoptosis after acute optic nerve injury. Tranpterional approach to decompression of optic canal has protective effect on RGC after acute optic nerve injury. Continuous application of dexamethasone after optic nerve injury has protective effect on RGC. The treatment and application of dexamethasone through pterional approach to decompression of optic canal can reduce the acute increase of TNF- 偽 concentration after acute optic nerve injury.
【學(xué)位授予單位】：新疆醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2012
【分類號(hào)】：R779.1

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