CAJ | 학술논문

目的探讨重组人碱性成纤维细胞生长因子( recombinant human basic fibroblast growth factor, rh-bFGF)对兔视网膜缺血再灌注损伤( retinal ischemia reperfusion injury, RIRI)的保护作用。方法选取健康纯种大耳白兔66只,随机分为假手术组6只,RIRI组30只,rh-bFGF组30只。通过升高眼压的方法制作兔RIRI模型,RIRI组予0.9%氯化钠注射液,rh-bFGF组予rh-bFGF治疗,假手术组仅用5号头皮针从耳前方角巩膜缘内刺入前房,之后缓慢拔除针头。 RIRI组和rh-bFGF组在RIRI后6 h、12 h、24 h、48 h、72 h常规HE染色观察视网膜组织形态变化,SABC免疫组织化学法检测视网膜组织中凋亡抑制基因Bcl-2和促凋亡基因Bax蛋白表达及Bcl-2/Bax的变化。结果假手术组视网膜未见凋亡细胞；RIRI组视网膜凋亡细胞主要出现在内核层和神经节细胞层,且在24 h达到高峰；rh-bFGF组与RIRI组比较,观察各时间点细胞损伤情况基本相似。 Bcl-2和Bax在正常视网膜组织中几乎不表达,在RIRI后6 h开始表达,24 h达到高峰,48 h开始下降,72 h后表达明显减弱。 rh-bFGF组与RIRI组比较,Bcl-2表达明显增强,而Bax表达减弱(P均<0.05)。结论 Bcl-2和Bax参与了RIRI的调控,rh-bFGF可通过上调Bcl-2表达及下调Bax表达,使Bcl-2/Bax比值升高,起到保护视网膜组织的作用。
목적탐토중조인감성성섬유세포생장인자( recombinant human basic fibroblast growth factor, rh-bFGF)대토시망막결혈재관주손상( retinal ischemia reperfusion injury, RIRI)적보호작용。방법선취건강순충대이백토66지,수궤분위가수술조6지,RIRI조30지,rh-bFGF조30지。통과승고안압적방법제작토RIRI모형,RIRI조여0.9%록화납주사액,rh-bFGF조여rh-bFGF치료,가수술조부용5호두피침종이전방각공막연내자입전방,지후완만발제침두。 RIRI조화rh-bFGF조재RIRI후6 h、12 h、24 h、48 h、72 h상규HE염색관찰시망막조직형태변화,SABC면역조직화학법검측시망막조직중조망억제기인Bcl-2화촉조망기인Bax단백표체급Bcl-2/Bax적변화。결과가수술조시망막미견조망세포；RIRI조시망막조망세포주요출현재내핵층화신경절세포층,차재24 h체도고봉；rh-bFGF조여RIRI조비교,관찰각시간점세포손상정황기본상사。 Bcl-2화Bax재정상시망막조직중궤호불표체,재RIRI후6 h개시표체,24 h체도고봉,48 h개시하강,72 h후표체명현감약。 rh-bFGF조여RIRI조비교,Bcl-2표체명현증강,이Bax표체감약(P균<0.05)。결론 Bcl-2화Bax삼여료RIRI적조공,rh-bFGF가통과상조Bcl-2표체급하조Bax표체,사Bcl-2/Bax비치승고,기도보호시망막조직적작용。
Objective To explore the protective effect of recombinant human basic fibroblast growth factor (rh-bFGF) on retinal ischemia-reperfusion injury (RIRI) in rabbits. Methods The 66 healthy purebred rabbits were randomly divided into sham-operation group (n=6), ischemia-reperfusion model group (n=30) and rh-bFGF treatment group (n=30). The RIRI models were established by elevating intraocular pressure, the ischemia-reperfusion model group was injected with 0. 9% sodium chloride injec-tion;rh-bFGF drug therapy was performed in rh-bFGF treatment group;the sham-operation group only received the 5th scalp heedle from ear piercing the anterior chamber angle in front of the sclera edge, and then the needle was slowly removed. Retina histopatho-logical changes were observed by routine hematoxylin and eosin stain 6 h, 12 h, 24 h, 48 h and 72 h after RIRI in ischemia-reperfu-sion model and rh-bFGF treatment groups. Expressions of inhibiting gene Bcl-2 and stimulative gene Bax and changes of Bax/Bcl-2 in retinal tissues were detected with SABC immunohistochemical method. Results No apoptotic cell was found in sham-operation group;apoptotic cells mainly existed in the inner nuclear layer and the ganglion cell layer, and apoptotic cells reached the peak 24 h after reperfusion;the rh-bFGF treatment groups had the similar condition with the ischemia-reperfusion model group in cell in-jury at each observational time. No expressions of Bcl-2 and Bax positive cells were found in normal retina tissues;the expressions were found 6 h after reperfusion, and the expressions reached the peak 24 h after reperfusion, and began to descented 48 h after reperfusion, and the decrease was obvious 72 h after reperfusion. Bcl-2 expression was significantly stronger, while Bax expression was significantly reduced in rh-bFGF treatment group, compared with those in ischemia-reperfusion model group (P<0. 05). Con-clusion Bcl-2 and Bax protein are involved in the RIRI regulation. The retina tissue can be protected with Bcl-2 expression of up-regulation and the Bax expression of down-regulation by rh-bFGF, which can increase the Bcl-2 /Bax ratio.