本文選題：視神經(jīng)損傷 + 谷氨酸��； 參考：《華中科技大學》2011年博士論文

【摘要】：目的利用質(zhì)子磁共振波譜(1H magnetic resonance spectroscopy,1H-MRS)研究視神經(jīng)橫切(optic nerve transection, ONT)大鼠視網(wǎng)膜代謝物質(zhì)的改變。 方法成年SD大鼠雙側(cè)上丘注射2%熒光金逆行標記視網(wǎng)膜神經(jīng)節(jié)細胞(retinal ganglion cells, RGCs)。熒光金標記后三天,將大鼠單側(cè)視神經(jīng)橫切離斷作為實驗組。對照組大鼠未行視神經(jīng)橫切。視神經(jīng)橫切后2周,處死大鼠,分離視網(wǎng)膜。行視網(wǎng)膜鋪片觀察RGCs的平均密度。利用質(zhì)子磁共振波譜研究大鼠視網(wǎng)膜提取物代謝物質(zhì)的變化。免疫組織化學染色觀察視網(wǎng)膜谷氨酸(glutamate,Glu),γ氨基丁酸(y-aminobutyric acid, GABA)和膠質(zhì)纖維酸性蛋白(glial fibrillary acidic protein, GFAP)的表達。 結(jié)果視神經(jīng)橫切組與對照組相比,視網(wǎng)膜GABA、N-乙酰天門冬氨酸(N-acetylaspartate,NAA)、�；撬�(taurine, Tau)、肌酸(creatine, Cr)濃度顯著下降,丙氨酸(alanine, Ala)濃度顯著升高。Glu、谷氨酰胺(glutamine, Gln)和Glx(Glu+Gln)濃度無統(tǒng)計學差異。對照組RGCs平均密度為2249±87/mm2,視神經(jīng)橫切組RGCs平均密度為320±56/mm2。與對照組相比,視神經(jīng)橫切組視網(wǎng)膜Glu和GABA免疫表達減弱,GFAP免疫表達顯著增強。 結(jié)論視神經(jīng)橫切后的RGCs死亡不僅與谷氨酸能和γ氨基丁酸能系統(tǒng)循環(huán)失衡有關(guān),而且同時伴隨其他的代謝物質(zhì)平衡失調(diào)。質(zhì)子磁共振波譜為我們提供了一個檢測視網(wǎng)膜代謝變化的有效方法,這些代謝物質(zhì)的變化為研究視神經(jīng)橫切后的RGCs死亡機制和神經(jīng)保護提供了重要的依據(jù)。 目的觀察金絲桃素對視神經(jīng)損傷大鼠視網(wǎng)膜神經(jīng)節(jié)細胞存活的作用。 方法將24只Sprague-Dawly (SD)大鼠隨機分成正常對照組,單純夾傷組,金絲桃素治療組和生理鹽水對照組。每組12只眼。大鼠雙側(cè)上丘注射2%熒光金逆行標記視網(wǎng)膜神經(jīng)節(jié)細胞,7d后對除正常對照組以外其他各組進行球后視神經(jīng)鉗夾處理,同時玻璃體內(nèi)分別注入金絲桃素或生理鹽水5μL,14d后進行視網(wǎng)膜鋪片和視網(wǎng)膜神經(jīng)節(jié)細胞的計數(shù)。 結(jié)果視神經(jīng)夾傷后14d存活的視網(wǎng)膜神經(jīng)節(jié)細胞數(shù)量顯著減少。單純夾傷組視網(wǎng)膜神經(jīng)節(jié)細胞存活率為50%,生理鹽水對照組視網(wǎng)膜神經(jīng)節(jié)細胞存活率為52%,金絲桃素治療組視網(wǎng)膜神經(jīng)節(jié)細胞存活率為68%。金絲桃素治療組相比單純夾傷組和生理鹽水對照組,存活的視網(wǎng)膜神經(jīng)節(jié)細胞明顯要多(P0.05)。 結(jié)論玻璃體內(nèi)注射金絲桃素不僅無毒副作用,而且能減少大鼠視神經(jīng)夾傷后誘發(fā)的視網(wǎng)膜神經(jīng)節(jié)細胞的死亡,對視網(wǎng)膜神經(jīng)節(jié)細胞有保護作用。金絲桃素可能為視神經(jīng)保護的新藥研究帶來新的思路。 目的觀察視神經(jīng)夾傷大鼠晶狀體損傷對視網(wǎng)膜神經(jīng)節(jié)細胞存活和軸突再生的影響。 方法將SD大鼠隨機分成正常組、對照組和處理組。正常組不做任何處理。對照組行單純雙眼視神經(jīng)鉗夾。處理組視神經(jīng)鉗夾后,雙眼玻璃體注射5μL生理鹽水,依據(jù)注射方式的不同分為晶狀體損傷組和晶狀體未損傷組。7d后大鼠雙側(cè)上丘注射熒光金,14d時行視網(wǎng)膜鋪片和冰凍切片,進行視網(wǎng)膜神經(jīng)節(jié)細胞計數(shù)。并用免疫組織化學檢測視網(wǎng)膜生長相關(guān)蛋白43(growth associated protein-43, GAP-43)和膠質(zhì)纖維酸性蛋白(glial fibrillary acidic protein, GFAP)的表達。 結(jié)果正常組和對照組的視網(wǎng)膜神經(jīng)節(jié)細胞計數(shù)分別為1987±154個·mm-2和908±123個·mm-2,處理組中的晶狀體損傷組和晶狀體未損傷組的視網(wǎng)膜神經(jīng)節(jié)細胞計數(shù)分別為1206±134個·mm-2和800±112個·mm-2。晶狀體損傷組存活的視網(wǎng)膜神經(jīng)節(jié)細胞數(shù)比對照組和晶狀體未損傷組多,差異有統(tǒng)計學意義(P0.05)。免疫組織化學顯示晶狀體損傷組視網(wǎng)膜GAP-43和GFAP的表達亦比對照組和晶狀體未損傷組增強。 結(jié)論晶狀體損傷能促進視神經(jīng)鉗夾傷大鼠視網(wǎng)膜神經(jīng)節(jié)細胞的存活,并增強視網(wǎng)膜GAP-43和GFAP的表達,促進軸突的再生。 目的探討視神經(jīng)炎患者的視野、視覺誘發(fā)電位、眼底熒光血管造影和影像學等檢查表現(xiàn)及臨床治療效果。 方法100例視神經(jīng)炎患者,分別行視野、視覺誘發(fā)電位、眼底熒光血管造影和影像學檢查,并給予糖皮質(zhì)激素、B族維生素、營養(yǎng)神經(jīng)類藥物、血管擴張劑及復方樟柳堿等綜合治療,觀察各項檢查表現(xiàn)及臨床治療效果。 結(jié)果大多數(shù)視神經(jīng)炎患者找不到明顯發(fā)病誘因,視野、視覺誘發(fā)電位和眼底熒光血管造影有相應的非特異性異常表現(xiàn),影像學檢查特別是磁共振有助于發(fā)現(xiàn)隱匿的異常病灶,有重要的臨床價值。經(jīng)綜合治療后,85例視力提高,15例視力不變或下降。 結(jié)論聯(lián)合各項檢查手段及時診斷及采取綜合治療是提高視神經(jīng)炎患者療效和預后的關(guān)鍵。
[Abstract]:Objective to study the changes of retinal metabolites in rat optic nerve transection (optic nerve transection, ONT) by means of 1H magnetic resonance spectroscopy (1H-MRS).
Methods adult SD rats with bilateral SC injection of 2% Fluorogold retrograde labeled retinal ganglion cells (retinal ganglion cells, RGCs). After three days of fluorescent gold labeling, the rats with unilateral optic nerve transection severed as the experimental group. The rats in control group without optic nerve transection. 2 weeks after optic nerve transection, death rat, isolated retina. The average density of retinal flatmount to observe the RGCs. Using the changes of metabolism of proton magnetic resonance spectroscopy study of retinal extract in rats. Immunohistochemical staining was used to observe the retinal glutamate (glutamate, Glu), gamma aminobutyric acid (Y-aminobutyric, acid, GABA) and glial fibrillary acidic protein (glial fibrillary acidic protein. The expression of GFAP).
Results the optic nerve transection group compared with control group, retinal GABA, N- acetylaspartate (N-acetylaspartate, NAA), taurine (taurine, Tau), creatine (creatine, Cr) were significantly decreased (alanine, Ala), alanine concentration significantly increased.Glu, glutamine (glutamine, Gln and Glx (Glu+Gln)) there was no significant difference in the control group RGCs concentration. The average density was 2249 + 87/mm2, optic nerve transection group average RGCs density was 320 + 56/mm2. compared with the control group, the optic nerve section group of retinal Glu and GABA immune expression decreased, GFAP expression was significantly enhanced.
Conclusion optic nerve after transection of the RGCs death not only with glutamatergic and GABAergic system cycle imbalance, and at the same time with other metabolic disorders. The material balance of proton magnetic resonance spectroscopy provides a useful method for the detection of retinal metabolic changes in the US, provides an important basis for the changes of these metabolites for optic nerve transection after studying the RGCs mechanism of death and neuroprotection.
Objective To observe the effect of hypericin on the survival of retinal ganglion cells in rats with optic nerve injury.
Methods 24 Sprague-Dawly (SD) rats were randomly divided into normal control group, simple injury group, hypericin treatment group and saline control group. Each group consisted of 12 eyes. Bilateral superior colliculus injection of 2% Fluorogold retrograde labeled retinal ganglion cells after 7d, except the normal control group to other groups of ball the visual nerve, and vitreous body were injected hypericin or saline 5 L, 14d after counting the retinas and retinal ganglion cells.
The results of optic nerve injury 14d survival of retinal ganglion cell numbers decreased significantly. The simple crush group of retinal ganglion cell survival rate was 50%, the saline control group of retinal ganglion cell survival rate was 52%, hypericin treatment group of retinal ganglion cell survival rate was 68%. hypericin treatment group compared with the injury group and normal the saline control group, the survival of retinal ganglion cells was significantly higher (P0.05).
Conclusion intravitreal injection of hypericin has no toxic side effect, and can reduce the death of rat retinal ganglion cells induced by optic nerve injury, has a protective effect on retinal ganglion cells. Hypericin may bring a new way of thinking for the research of new drugs of optic nerve protection.
Objective To observe the effect of lens injury on retinal ganglion cell survival and axonal regeneration in rats with optic nerve clamp injury.
Methods SD rats were randomly divided into normal group, control group and treatment group. The normal group without any treatment. The control group underwent bilateral optic nerve optic nerve. Treatment group after injection, eyes vitreous body 5 L normal saline, according to different injection methods for the damage of lens group and lens injury group without.7d after bilateral superior colliculus injection of fluorogold, 14d underwent retinal flatmount and frozen sections of retinal ganglion cell count. And immunohistochemical detection of retinal growth associated protein 43 (growth associated, protein-43, GAP-43) and glial fibrillary acidic protein (glial fibrillary acidic protein, GFAP) expression.
Results retinal ganglion cell count in normal group and control group were 1987 + 154 and 908 + 123 - mm-2 - mm-2, retinal ganglion cell count in the treatment group of lens injury group and lens without injury group were 1206 + 134 and 800 + 112 - mm-2 - mm-2. lens injury group the survival of retinal ganglion cell number compared with the control group and the non lens injury group, the difference was statistically significant (P0.05). Immunohistochemistry showed that the expression of GAP-43 in retina and lens injury group GFAP than control group and injury group lens were not enhanced.
Conclusion lens injury can promote the survival of retinal ganglion cells and enhance the expression of GAP-43 and GFAP in retina, and promote axonal regeneration.
Objective to investigate the visual field, visual evoked potential, fundus fluorescein angiography and imaging, and the clinical therapeutic effect of optic neuritis.
Methods 100 cases of optic neuritis patients underwent vision, visual evoked potential, fundus fluorescein angiography and imaging examination, and glucocorticoid, B vitamins, neurotrophic drugs, vasodilators and compound anisodine combined therapy, observe the inspection findings and clinical therapeutic effect.
Results most patients with optic neuritis have no obvious inducement, vision, visual evoked potential and fundus fluorescein angiography have corresponding nonspecific abnormalities, especially magnetic resonance imaging examination is helpful to find abnormal lesions occult, has important clinical value. After comprehensive treatment, visual acuity was improved in 85 cases, 15 cases of visual acuity constant or decreased.
Conclusion it is the key to improve the curative effect and prognosis of patients with optic neuritis to diagnose and take comprehensive treatment in time.

【學位授予單位】：華中科技大學
【學位級別】：博士
【學位授予年份】：2011
【分類號】：R774.61

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