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神經(jīng)生長因子對青光眼視神經(jīng)保護(hù)的臨床觀察

發(fā)布時間:2018-05-27 21:33

  本文選題:神經(jīng)生長因子 + 原發(fā)性閉角型青光眼; 參考:《鄭州大學(xué)》2010年碩士論文


【摘要】: 背景和目的 青光眼是一組以視神經(jīng)萎縮和視野缺損為共同特征的多因素、進(jìn)展性神經(jīng)退化疾病。視網(wǎng)膜神經(jīng)節(jié)細(xì)胞(retinal ganglion cell, RGCs)進(jìn)行性喪失是其共同的病理改變。眼內(nèi)壓的升高是青光眼最為顯著的危險因素,因此,當(dāng)前大部分的治療都是圍繞降低眼內(nèi)壓來開展的。然而,眼壓控制良好的青光眼患者仍然會發(fā)生視野缺損的惡化和RGCs的死亡。因此,需要一種附加的治療已經(jīng)得到了廣泛的認(rèn)可。 隨著青光眼視神經(jīng)損傷動物模型研究領(lǐng)域的飛速發(fā)展,我們對青光眼的病理過程的認(rèn)識也在不斷提高。視神經(jīng)保護(hù)藥物的作用在這些實驗基礎(chǔ)上表現(xiàn)出越來越多的優(yōu)越性,神經(jīng)生長因子(nerve growth factor, NGF)作為一種重要的生物活性分子廣泛作用于中樞和周圍的神經(jīng)元。近年來青光眼動物模型研究已經(jīng)證實,外源性NGF與其受體結(jié)合一方面可以通過清除氧自由基,阻止谷氨酸引起的興奮性毒作用以及穩(wěn)定細(xì)胞內(nèi)Ga2+濃度抑制RGCs凋亡;另一方面通過激活不同的信號傳導(dǎo)通路,促進(jìn)RGCs及軸突的發(fā)育和損傷后再生。本研究擬通過觀察神經(jīng)生長因子(NGF)對原發(fā)性閉角型青光眼患者血漿內(nèi)皮素(endothelin,ET)、血清一氧化氮(nitric oxide, NO)、視力、眼壓、視野、視覺電生理(visual evoked potential, VEP)等指標(biāo)的影響,進(jìn)一步探討其作用機(jī)制,為青光眼臨床預(yù)防和治療工作提供新的思路。 方法 本研究選擇2008年12月至2009年10月間,在鄭州大學(xué)第一附屬醫(yī)院眼科檢查,臨床確診為原發(fā)性閉角型青光眼,住院后行小梁切除術(shù)治療的患者。符合上述標(biāo)準(zhǔn)共56例(56眼)。56例病例中,男性24例,女性32例,年齡41~68歲,中位年齡54.3±7.97。其中8例雙眼均行手術(shù)患者,取術(shù)后矯正視力較好眼為觀察眼。隨機(jī)分為NGF治療組29例(29眼)與甲鈷胺對照組27例(27眼)。治療組術(shù)后給予注射用鼠神經(jīng)生長因子治療,對照組術(shù)后常規(guī)口服甲鈷胺片。測定各組治療前、后及1月后復(fù)查的視力、眼壓、視野、視覺誘發(fā)電位(VEP)指標(biāo)、血漿ET-1和血清NO水平。 所有數(shù)據(jù)用均數(shù)±標(biāo)準(zhǔn)差表示,數(shù)據(jù)統(tǒng)計分析由SPSS17.0軟件完成。對于組內(nèi)比較采用t檢驗,同期組間比較采用單因素方差分析。計數(shù)資料采用χ2檢驗。取α=0.05為檢驗水準(zhǔn),以P0.05為差異具有統(tǒng)計學(xué)意義。 結(jié)果 1.NGF組患者治療前、后及復(fù)查時的視力與同期對照組對比差異無統(tǒng)計學(xué)意義(P0.05),1m復(fù)查視力較治療前顯著增加(P0.05)。 2.NGF組患者治療前、后及復(fù)查的眼壓與同期對照組對比差異均無統(tǒng)計學(xué)意義(P0.05)。 3.NGF組患者治療后及復(fù)查視野MS、P100振幅、血清NO水平均較同期對照組顯著增加(P0.05),視野MD、P100潛伏期和血漿ET-1水平顯著低于同期對照組(P0.05)。 結(jié)論 1.對于眼壓控制良好的青光眼患者,NGF可以促進(jìn)部分視神經(jīng)功能的恢復(fù)。 2.NGF可能存在一種長效機(jī)制,在復(fù)查時視野、視力、電生理參數(shù)的改善仍在持續(xù)。 3.NGF對青光眼患者的眼壓無明顯影響。 4.NGF視神經(jīng)保護(hù)機(jī)制可能與其對ET/NO的影響有關(guān)。
[Abstract]:Background and purpose
Glaucoma is a group of factors with the common characteristics of optic atrophy and visual field defect, progressive neurodegenerative disease. The progressive loss of retinal ganglion cell (RGCs) is a common pathological change. The increase of intraocular pressure is the most significant risk factor for glaucoma. Therefore, most of the current treatments are However, glaucoma patients with well controlled intraocular pressure still suffer from deterioration of the visual field and the death of RGCs. Therefore, the need for an additional treatment has been widely recognized.
With the rapid development of the research field of the animal model of optic nerve injury in glaucoma, our understanding of the pathological process of glaucoma is also increasing. The role of optic neuroprotective drugs has shown more and more advantages on these experiments. Nerve growth factor (NGF) is an important bioactive component. In recent years, the combination of exogenous NGF and its receptor has proved that the combination of exogenous NGF and its receptor can eliminate oxygen free radicals, prevent excitatory effects caused by glutamic acid, and stabilize intracellular Ga2+ concentration to inhibit RGCs withering; on the other hand, different signal transmission is activated by activating different signals. This study aims to observe the effects of neural growth factor (NGF) on plasma endothelin (endothelin, ET), serum nitric oxide (nitric oxide, NO), vision, intraocular pressure, visual field, visual electrophysiology (visual evoked potential, VEP) in patients with primary angle closure glaucoma. Objective to explore the mechanism of action and provide new ideas for clinical prevention and treatment of glaucoma.
Method
This study was conducted from December 2008 to October 2009 at the First Affiliated Hospital of Zhengzhou University. Patients with primary angle closure glaucoma and trabeculectomy after hospitalization were treated in the First Affiliated Hospital of Zhengzhou University. Of the 56 cases (56 eyes), 24 cases, 32 women, 41~68 years of age and 8 age of 54.3 + 7.97. of the median age were 8. Cases of both eyes were performed, and the corrected visual acuity was observed. 29 cases (29 eyes) and Mecobalamin control group were randomly divided into 29 cases (29 eyes) and 27 cases of mecobalamin control group (27 eyes). The treatment group was treated with Mouse Nerve Growth Factor for Injection after operation, and the control group was given the routine oral Mecobalamin Tablets after operation. The visual acuity and intraocular pressure were determined before and after January. Visual field, visual evoked potential (VEP), plasma ET-1 and serum NO levels.
All data were expressed with mean standard deviation, and data statistical analysis was completed by SPSS17.0 software. T test was used in group comparison, single factor analysis of variance was used in the same period. The count data was tested by x 2 test. Alpha =0.05 was taken as the test level, and P0.05 was statistically significant.
Result
There was no significant difference in visual acuity before and after treatment between the 1.NGF group and that of the control group (P0.05). The visual acuity of 1m reexamination increased significantly compared with that before treatment (P0.05).
There was no significant difference in the intraocular pressure before and after treatment in group 2.NGF compared with that in the control group (P0.05).
After treatment and reexamination of the 3.NGF group, the MS, P100 amplitude and serum NO level were significantly higher than those in the control group (P0.05), the visual field MD, the P100 latency and the plasma ET-1 level were significantly lower than those in the control group (P0.05).
conclusion
1. NGF can promote the recovery of some optic functions in glaucoma patients with good intraocular pressure control.
There may be a long-term mechanism for 2.NGF, which improves the visual acuity and electrophysiological parameters during reexamination.
3.NGF has no significant effect on intraocular pressure in patients with glaucoma.
The mechanism of 4.NGF's optic nerve protection may be related to its effect on ET/NO.
【學(xué)位授予單位】:鄭州大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2010
【分類號】:R775

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 郭巖;地塞米松對大鼠坐骨神經(jīng)損傷后骨骼肌及運(yùn)動終板修復(fù)作用的研究[D];青島大學(xué);2011年

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