全反式维甲酸对翼状胬肉成纤维细胞增殖的影响

目的:观察全反式维甲酸(ATRA)对体外培养人翼状胬肉成纤维细胞(HPF)增殖的影响,寻找治疗和预防翼状胬肉复发的新途径。方法:体外培养翼状胬肉患者成纤维细胞;将不同浓度的ATRA作用于成纤维细胞分别达24,48h和72h后,MTT法检测ATRA对HPF的影响,免疫组织化学染色增生细胞核抗原(PCNA)检测细胞生长活性。结果:MTT法显示10-8mmol/LATRA作用24h后能抑制HPF的增殖(P<0.05),呈剂量和时间依赖性。ATRA能浓度依赖性地抑制细胞表达PCNA(P<0.05)。结论:ATRA能够显著抑制HPF的增殖。     

羟基喜树碱对培养的兔晶状体上皮细胞的影响

目的 探讨羟基喜树碱（hydroxycamptothecine,HCPT)对兔晶状体上皮细胞（rabbit lens epithelial,RLECs)细胞周期的阻断作用和诱导细胞凋的作用,并研究其对Fas/FasL表达的影响。方法 使用流式细胞仪分析检测HCPT对RLECs细胞周期的阻断作用,以光镜和电子显微镜观察细胞形态的变化,应用末端脱氧核酸转移酶介导的脱氧三磷酸尿苷缺口末端标记法检测HCPT诱导的细胞凋亡情况,应用免疫组化方法检测HCPT对Fas/FasL表达的影响。结果 HCPT可将RLECs阻断于细胞周期的S期并诱导其凋亡;凋亡细胞具有典型的形态;脱氧尿苷三磷酸标记显示散在阳性细胞,且凋亡细胞的数量随HCPT药物浓度的增加而增多。HCPT对RLECs的Fas/FasL表达无明显影响。结论 HCPT不仅可阻断RLECs的分裂,而且可诱导细胞发生凋亡;Fas/FasL介导途径未参与HCPT诱发RLECs凋亡的过程。     

紫杉醇诱导兔晶状体上皮细胞凋亡及细胞周期改变的研究

目的 探讨紫杉醇(Taxol)诱导兔晶状体上皮细胞(RLECs)凋亡和对细胞周期改变的作用以及对Fas和FasL基因表达的影响。方法 流式细胞仪分析检测Taxol诱导RLECs细胞周期的阻断；光镜和电子显微镜下观察细胞形态的变化；应用TUNEL法检测药物诱导的细胞凋亡；兔疫组化方法检测该药对Fas和FasL基因的表达。结果Taxol可将RLECs阻断于G2／M期并诱导其凋亡；可见凋亡小体；TUNEL染色显示散在的阳性细胞，且凋亡的细胞量随药物质量浓度的增加而增多；Taxol对RLECs的Fas及FasL基因的表达无明显影响。结论 Taxol不仅能阻断RLECs的分裂，还能诱导其发生细胞凋亡，但不是通过Fas／FasL途径介导的。     

表皮生长因子对人视网膜色素上皮细胞增生及移行的影响

目的　观察表皮生长因子 (epidermalgrowthfactor,EGF)及血清对体外培养的人视网膜色素上皮 (retinalpigmentepithelium ,RPE)细胞增生及移行的影响。 方法　对培养的人 3～ 6代RPE细胞采用MTT比色法观察不同浓度的EGF(0 .1、1、10、5 0、10 0 μg·L-1)及血清对人RPE细胞增生的影响 ;应用RPE细胞损伤模型 ,计数进入缺损区的细胞 ,定量观察EGF及血清对RPE细胞移行的影响。结果　在细胞增生的实验中 :无血清组 ,10～ 10 0 μg·L-1EGF达到最佳刺激浓度 ,其增生率为 81.8% ;5 0mL·L-1血清组 ,1～10 μg·L-1EGF的刺激作用最强达到 12 2 .7% ;无血清组与 5 0mL·L-1血清组间有显著性差异 (P <0 .0 0 1) ,且 5 0mL·L-1血清可明显促进人RPE细胞的增生 (P <0 .0 0 1)。在细胞的移行实验中 :无血清组 ,1～ 10 0 μg·L-1EGF可促进RPE细胞移行 ,但作用较弱 ;10 0mL·L-1血清组中 1～ 10 μg·L-1EGF促移行作用最强达 4 38.9% ;1～ 10 0 μg·L-1EGF的促进基础RPE细胞移行能力 (最强为 36 % )低于 10 0mL·L-1血清诱导的RPE细胞的移行能力 (强度为 14 7% ) ;无血清组与 10 0mL·L-1血清组间有显著性差异 (P <0 .0 0 1)。结论　EGF对体外培养的人RPE细胞具有浓度依赖性促增生和移行的作用 ;血清自身也具有此作用     

环孢素A对兔晶状体上皮细胞增殖的影响

目的研究环孢素A(CsA)在不同情况下,对兔晶状体上皮细胞(RLECs)超微结构和增殖的影响。方法用CsA分别处理正常生长的RLECs和经过H2O2损伤的RLECs后,用透射电镜观察RLECs超微结构变化;噻唑蓝(MTT)法测定RLECs增殖能力改变。结果CsA浓度≥10μmol/L时,明显损伤正常RLECs的超微结构和增殖;当浓度<40μmol/L时,能部分抑制H2O2对RLECs超微结构损伤和增殖抑制。与对照组比较,差异有显著意义(P<0.01)。结论CsA对不同情况下的兔晶状体上皮细胞的超微结构和增殖具有不同的作用。     

人视网膜色素上皮细胞在电场中定向移行的实验研究

目的:观察外源性电场对培养人视网膜色素上皮humanretinalpigmentepithelial,hRPE)细胞移行方向及细胞内肌动蛋白表达的影响。方法:培养于DMEM+100g/LFBS的hRPE细胞暴露于强度为6V/cm的电场中,未暴露于电场的细胞作为对照。观察并记录2h中每隔15min细胞移行的变化图像,测量细胞移行距离、细胞移行方向及其与场线间夹角。2h后采用间接免疫荧光法检测实验组与对照组细胞内肌动蛋白表达情况。SPSS10.0及Image-ProPlus5.0软件处理结果。结果:未暴露于电场中的hRPE细胞在观察期间呈无序移行,2h后细胞分布未见特殊变化,细胞内肌动蛋白有弱阳性表达。细胞暴露于电场30min后开始出现阴极方向的移行趋势,大部分细胞长轴趋向垂直于场线方向排列。细胞的移行表现为移行速度和移行方向的一致性均随时间延长而增加(P<0.05)。暴露于电场2h后,大部分细胞内肌动蛋白表达阳性,且多集中分布于细胞质内朝向电场阴极一侧。结论:外加电场可诱导hRPE细胞向电场阴极方向定向移行,同时伴有细胞内肌动蛋白阳性表达及定向分布。电场对细胞的作用与暴露时间成正相关。视网膜脱离后的内源性电场的存在可能参与并诱导了RPE细胞的定向移行。     

纤维连接蛋白对人晶状体上皮细胞系的增殖、黏附和移行的影响

目的:探讨纤维连接蛋白(fibronectin,FN)对人晶状体上皮细胞系HLE-B3的增殖、黏附和移行的影响及其受体整合素α5亚基的表达。方法:培养人晶状体上皮细胞系HLE-B3,接种于不同浓度的FN(0,10,20,40mg/L)包被的培养板中,倒置显微镜下观察HLE-B3的生物学特性,采用WST-8法检测细胞的增殖、黏附情况,划痕法观察细胞的移行并记录细胞缺损区闭合时间,免疫细胞化学法观察整合素α5亚基的表达。结果:各浓度FN包被后,增殖实验中WST-8法检测的吸光值增高不明显(P>0.05)。随FN包被浓度的增高,黏附实验中的吸光值逐渐增高,划痕实验中缺损区闭合的时间逐渐缩短,各浓度组在统计学上具有显著性差异。整合素α5亚基随FN包被浓度的增高表达增强(P<0.05)。结论:FN具有显著促进HLE-B3黏附和移行的作用,同时能上调其受体整合素α5亚基的表达。     

层粘连蛋白在大鼠角膜碱烧伤中的表达及意义

目的　研究层粘连蛋白 (laminin ,LN)在大鼠角膜碱烧伤模型中表达的变化 ,揭示其在角膜碱烧伤修复过程中的作用。方法　制作大鼠角膜碱烧伤模型 ,以免疫组化的方法观察LN在烧伤后 12h、2 4h、3d、7d、14d时表达的变化。结果　LN在正常大鼠角膜仅在基底层柱状上皮细胞胞浆和胞间以及基底膜有少许表达 ;烧伤后 12h ,基底柱状上皮细胞胞浆和胞间以及基底膜的表达增多 ,同时角膜基质层、角膜固有细胞出现LN ,并于 3～ 7d达高峰 ;14d角膜修复时 ,在基底膜柱状细胞、基质中表达减少 ,在角膜基质中表达基本消失。结论　LN在角膜碱烧伤过程中扮演重要角色 ,在介导淋巴细胞吞噬坏死组织、介导细胞 细胞间、细胞 细胞外基质间的黏附、介导上皮细胞移行中有重要作用 ,对于角膜的重新上皮化有积极作用。     

白细胞介素-1β促人视网膜色素上皮细胞分泌细胞间黏附分子和整合素β1

增生性玻璃体视网膜病变（PVR）的病程进展与细胞粘附、移行和增生的能力密切相关。细胞黏附分子（CAMs）中的整合素β1和细胞间黏附分子-1（ICAM-1）介导了细胞-基质及细胞-细胞间的相互作用，调节细胞的移行、分化和增生，与PVR相关性较大。我们选择二者作为研究对象，检测它们存炎性因子白细胞介素（IL）-1β作用下视网膜色素上皮（RPE）细胞中的表达情况，     

四种药物对兔晶状体上皮细胞的影响

目的观察利多卡因、丁卡因、透明质酸酶和肾上腺素对体外培养的兔晶状体上皮细胞（rabbit lens epithelial cells,RLECs）的影响。方法采用组织块培养法培养RLECs,分别用利多卡因、丁卡因、透明质酸酶和肾上腺素4种不同浓度的药物对细胞进行干预,以未加药物的培养液作为阴性对照,采用四甲基偶氮唑盐比色法（MTT法）检测药物对RLECs的影响,并用光镜和电镜来观察细胞形态结构变化。结果4种药物均可破坏细胞间及细胞与培养瓶底部之间的连接,使正常应该贴壁的RLECs从瓶壁脱落。除100U·L^-1透明质酸酶（P=0.0545）和10×10-6g·L^-1肾上腺素（P=0.4210）外,其余各实验组药物作用24h时均可明显抑制RLECs增生,且其抑制作用具有浓度和时间依赖性。作用24h时4种药物的半数抑制浓度（IC50）分别为：利多卡因组0.5g·L^-1,丁卡因组0.375g·L^-1,透明质酸酶组200×103U·L^-1,肾上腺素组0.1g·L^-1。4种药物在IC50下作用24h均可损伤RLECs,导致细胞死亡,以利多卡因组和丁卡因组作用较为显著。结论利多卡因、丁卡因、透明质酸酶和肾上腺素对体外培养的RLECs增生具有抑制作用,并可破坏细胞结构而导致细胞死亡。     

MTT比色法检测苦参碱对兔晶状体上皮细胞增生的影响

目的研究苦参碱对体外培养的兔晶状体上皮细胞增生的影响,探索白内障术后晶状体后囊浑浊的治疗药物。方法取第2代对数生长期的兔晶状体上皮细胞,培养24h后,加入不同浓度的苦参碱(0.1、0.2、0.4、0.6、0.8、1.0、1.2、1.4、1.6mg/mL)作用24h后,采用MTT法观察苦参碱对兔晶状体上皮细胞增生的影响。结果苦参碱随着浓度的增加,其抑制兔晶状体上皮细胞增生的作用逐渐增强,增生抑制率的升高呈现明显的剂量依赖性。结论苦参碱能有效抑制体外培养的兔晶状体上皮细胞增生,在防止白内障术后晶状体后囊浑浊方面有一定的应用前景。     

Effect of minoxidil on rabbit lens epithelial cell behavior in vitro and in situ

BACKGROUND: Lens epithelial cell (LEC) proliferation and the associated production of extracellular matrix (ECM) are responsible for capsular opacification after cataract-IOL surgery. Minoxidil is an inhibitor of lysyl hydroxylase, an enzyme involved in procollagen hydroxylation. To evaluate the potential efficacy of minoxidil in inhibiting postoperative capsular opacification, we examined the effects of minoxidil on LEC behavior in cell and organ cultures. METHODS: We examined minoxidil effects on collagen production, migration and proliferation of cultured rabbit LECs as well as its ultrastructural effects, and also its effects on the cell population in organ-cultured capsular bag. RESULTS: No cytotoxicity was identified by MTT assay at the concentrations up to 3.0 mM of minoxidil, whereas it decreased the collagen production in LECs. Minoxidil also inhibited migration and proliferation of cells. Ultrastructural observation revealed the presence of dilated endoplasmic reticulum in LECs treated with minoxidil, indicating the accumulation of protein, probably underhydroxylated collagen precursors. The capsules cultured with minoxidil appeared less opaque than control specimens. On histological examination the numbers of cells on equatorial capsules were found to be significantly lower in minoxidil culture than in control culture. No lens cells were detected on the central posterior capsule of minoxidil culture, whereas they were seen in control. CONCLUSION: Minoxidil inhibited LEC migration and proliferation in vitro, as well as collagen secretion. Collagen secretion may be essential for LEC migration and proliferation. Minoxidil also attenuated repopulation of LECs on the inner surface of organ-cultured capsules. Minoxidil may be a potential inhibitor of postoperative capsular opacification.     

Posterior capsule opacification

PURPOSE OF REVIEW: This paper assesses the factors that contribute to the formation of an effective capsular bend as a deterrent to posterior capsule opacification. Its goal is to assist the practicing ophthalmologist in separating current understanding of this process from various working models previously proposed. RECENT FINDINGS: While a square-edge design appreciably improves resistance to posterior capsule opacification, significant factors remain under the control of the surgeon. These factors combine to form the physical and psychological barrier of a capsular bend. Innovative digital imaging has shown lens epithelial cell migration, allowing for a more rapid assessment of posterior capsule opacification resistance. A three-piece intraocular lens allows for full 360 degree capsular bend formation surrounding the optic edge; some single-piece designs may inhibit capsular bend formation. Decreasing, but not eliminating, the surviving lens epithelial cell population may diminish capsular bend strength, which may decrease resistance to posterior capsule opacification in the face of a regenerating cortex. All demographic features of clear/refractive lens exchange suggest higher rates of posterior capsule opacification than with standard cataract surgery. SUMMARY: The quality of capsular bend formation will determine how resistant an intraocular lens will be to posterior capsule opacification as a consequence of regenerating cortex. As refractive lens exchange and new accommodating intraocular lens designs become more popular, the problems of regenerating cortex will increase in magnitude.     

Inhibitory effects of salmosin,a disintegrin,on posterior capsular opacification in vitro and in vivo

The proliferation, migration and transdifferentiation of the remaining lens epithelial cells (LECs) after cataract surgery are a major cause of posterior capsular opacification (PCO). It has previously been reported that salmosin, a novel disintegrin, significantly inhibits solid tumor growth in mice by perturbation of tumor-specific angiogenesis via blocking alpha v beta 3 integrin expressed on vascular endothelial cells. In this study, the inhibitory function of salmosin in PCO was investigated and was found that salmosin inhibits the attachment of bovine LECs and rabbit lens cells (N/N1003A) to extracellular matrix-coated plates. The anti-adhesive activity of salmosin was approximately 1000 times higher than that of synthetic Arg-Gly-Asp peptide. In addition, the cell proliferation and migration of bovine LECs and N/N1003A were strongly inhibited by salmosin, whereas the proliferation of corneal endothelial cells was less affected. LEC migration and proliferation were also decreased by salmosin treatment in rabbit eyes without any toxic effect in the cornea, iris and retina. In this study, salmosin was shown to specifically inhibit LEC migration and proliferation in an animal model. Therefore, the authors suggest that further investigation may show salmosin to be a good candidate for inhibiting PCO development.     

甘糖酯对囊袋法培养的兔晶状体上皮细胞增生的抑制作用

目的应用甘糖酯（PGMS）抑制囊袋法培养的兔晶状体上皮细胞（LECs）的增生和移行能力,探讨其对后发性白内障的预防和治疗作用。方法健康纯种白兔30只模拟白内障囊外摘出术（ECCE）建立兔LECs体外培养的囊袋模型,将制备好的囊袋浸泡于不同质量浓度的PGMS中分别作用不同时间。实验组分别用0.2、0.4、0.8g/LPGMS浸泡晶状体囊袋,作用时间分别为2、5、10min,空白对照组晶状体囊袋不用PGMS浸泡。囊袋置于含质量分数5%胎牛血清的DMEM培养液中培养。7d后以囊膜细胞覆盖率作为评价指标,观察兔LECs增生、移行情况;应用苏木精-伊红染色法进行组织病理学检查,观察LECs的形态及其与晶状体囊袋的结合情况;透射电镜下观察后囊膜上LECs的超微结构。结果对照组在培养的第3天可见LECs呈铺路石样生长,第7天后囊膜LECs的覆盖率达100%;各实验组LECs的覆盖率较对照组明显下降（P〈0.05）。实验组随着PGMS质量浓度的增加和作用时间的延长,细胞增生、移行的速度明显减慢,其中质量浓度为0.8g/L,作用时间5min和10min组显著抑制兔LECs生长,与对照组和0.2g/LPGMS培养组比较差异均有统计学意义（P〈0.05）。病理组织学检测表明0.4g/L及0.8g/LPGMS作用2min组晶状体后囊膜LECs数目较对照组和0.2g/LPGMS组明显减少,细胞与囊膜连接不紧密。透射电镜下可见对照组和0.2g/LPGMS组LECs结构完整;0.4g/L及0.8g/LPGMS组可见细胞内有较多溶酶体,细胞质空泡样变性等退行性改变。结论 PGMS对囊袋培养的兔LECs的增生、移行的抑制作用呈质量浓度及时间依赖性。     

兔眼IOL术后基质金属蛋白酶抑制因子在虹膜、晶状体上皮细胞的表达

目的　探讨白内障囊外摘出及人工晶状体植入术后基质金属蛋白酶抑制因子 (TIMPs)在虹膜、晶状体上皮细胞的表达和TIMPs对后囊膜混浊的形成及纤维化的影响。方法　取 2 5只健康成年家兔 ,均一只眼行晶状体囊外摘出及人工晶状体植入术 ,另一眼作为对照组。每 5只兔眼为一组 ,分别于术后 1、3、7、14、3 0d取出虹膜和晶状体上皮细胞 ,用RT PCR和反向酶谱分析法检测各标本中的TIMPsmRNA和蛋白质的表达 ,并用羟脯氨酸试剂盒检测晶状体囊膜羟脯氨酸量的变化。结果　在正常虹膜、晶状体上皮细胞组织均有TIMP 1、 2、 3和 4mRNA的表达 ,而无相对蛋白质活性的表达 ;术后第 1d ,TIMP 1、 2、 3和 4mRNA即出现明显升高 ,其中术后第 7d ,TIMP 1和 2mRNA的表达量为最大 ,此后逐渐下降 ,术后第 3 0d的表达量仍高于对照组 (P <0 0 5 ) ;TIMP 3mRNA轻度升高 ,TIMP 4mRNA则轻度下降 ;羟脯氨酸的含量于术后 1、3、7d和 14d明显低于术后 3 0d(P <0 0 5 )。结论　TIMPs可能是抑制白内障囊外摘出及人工晶状体植入术后细胞外基质降解的主要因素 ,还可能是后囊膜混浊的形成和纤维化的重要原因之一。     

Hepatocyte growth factor induces proliferation of lens epithelial cells through activation of ERK1/2 and JNK/SAPK

PURPOSE: Posterior capsule opacification (PCO) is caused by proliferation and migration of lens epithelial cells (LECs) remaining after cataract surgery. In this study, the effect of HGF in LECs and the signaling pathways that contribute to HGF-induced proliferation were investigated. METHODS: Capsular bags prepared from porcine eyes were maintained in serum-free DMEM. The human lens epithelial B3 cells (HLE B3) and rat lens epithelial explants were cultured in MEM supplemented with 20% FCS and medium 199 with 0.1% BSA, respectively. Cell proliferation was determined by MTT assay, proliferating cell nuclear antigen (PCNA) expression, or flow cytometry. An antisense oligonucleotide was used to inhibit cyclin D1 expression. Activation of the mitogen activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) pathways was detected by immunoblot analysis. RESULTS: The proliferation of LECs in a capsular bag culture was significantly inhibited by treatment with the neutralizing antibody for HGF receptor. Stimulation of HLE B3 with hepatocyte growth factor (HGF) activated the MAPKs, ERK, and JNK/SAPK, but not p38. Activation of both ERK and JNK/SAPK was necessary for the HGF-stimulated induction of cyclin D1, which in turn was necessary for the HGF-induced proliferation of LECs. PI3K also participated in the regulation of cyclin D1 expression upstream of ERK and JNK/SAPK. CONCLUSIONS: The data indicate that HGF is a potent growth factor for LECs and may contribute to the development of PCO and suggest that the signaling pathways involved in HGF-stimulated proliferation may constitute potential therapeutic targets in the treatment of PCO.     

An in vitro model of posterior capsular opacity: SPARC and TGF-beta2 minimize epithelial-to-mesenchymal transition in lens epithelium

PURPOSE: This report presents a novel model for studies of extracellular matrix (ECM) in posterior capsular opacification (PCO) in vitro. Lens epithelial cells (LEC) were cultured with an intraocular lens (IOL) on a surface of type IV collagen in an evaluation of the importance of the ECM-cell interaction in formation of PCO. Abnormal migration, proliferation, and expression of proteins associated with the epithelial-to-mesenchymal transition (EMT) that characterizes PCO were observed in the presence and absence of the matricellular protein SPARC (secreted protein, acidic and rich in cysteine), which regulates matrix-cell interactions. METHODS: The model for PCO in vitro consisted of an IOL placed on a membrane coated with collagen IV, a major constituent of the lens capsule. LECs from the lenses of wild-type (WT) and SPARC-null (SP-null) mice were cultured in the presence or absence of 10 ng/mL TGF-beta2 and 20 mug/mL recombinant human SPARC (rhSP) for up to 6 days. The migration of LECs was quantified. Labeling with BrdU and the measurement of DNA synthesis were assays for cell proliferation. Expression of the EMT markers, collagen type I, fibronectin, and alpha-smooth muscle actin were assessed using immunocytochemistry or Western immunoblots. RESULTS: LEC migration, proliferation, and the synthesis of EMT markers were enhanced in SP-null compared with WT LECs. TGF-beta2 inhibited the migration and proliferation of both WT and SP-null LECs in the presence of rhSP. TGF-beta2 increased the production of collagen type I, fibronectin, and alpha-SMA. The responses of SP-null LECs were rescued by the addition of recombinant human (rh)SP. CONCLUSIONS: A simple IOL culture system was useful for the evaluation of the effects of SPARC and TGF-beta2 on PCO in vitro. The action of TGF-beta2 on LEC migration and proliferation is influenced by SPARC, a regulator of matrix-cell interactions. The results indicate a functional intersection between pathways activated by TGF-beta2 and SPARC in the formation of PCO.     

大鼠后囊膜混浊模型的建立

目的建立一种新的、具有实用价值的大鼠后囊膜混浊(posterior capsule opacification,PCO)动物模型。方法12只SD(Sprague Dawley)大鼠随机分为4组,每组3只,每只大鼠双眼施行晶状体囊外摘除术(extracapsular lens extrac-tion,ECLE);在手术后即刻、第1天、第7天、第14天摘除眼球,进行组织病理学观察,研究残留晶状体上皮细胞(lensep-ithelial cells,LECs)增殖、移行和后囊膜的动态变化;应用方差分析比较LECs增殖数量。结果所有大鼠均成功施行ECLE手术。手术后即刻可见前囊膜下及赤道部有单层的LECs排列;术后第1天赤道部形成由2～3层细胞组成的细胞团块,LECs沿着囊膜向后囊迁移;术后第7天囊袋赤道部及后囊膜下形成多层细胞结构,赤道部晶状体纤维样物质增加,部分后囊膜出现明显皱褶;术后第14天囊袋赤道部及后囊膜下LECs形成团块,赤道部形成晶状体纤维样结构,赤道部Soemmering环形成。随时间推移,单位面积LECs数量明显增加(P<0.05)。结论大鼠ECLE手术后可成功建立后囊膜混浊模型。     

bFGF在体外培养的晶状体上皮细胞中的表达及对细胞周期的影响

目的　观察碱性成纤维细胞生长因子(bFGF)在体外培养的不同阶段小鼠晶状体上皮细胞(LECs)中的表达,及其对细胞周期的影响并探讨其机制。方法将昆明健康小鼠的晶状体前囊膜取出,做体外培养并传代。利用免疫组织化学法和Westernblot法检测bFGF在体外培养的不同阶段LECs中的表达情况,并利用流式细胞法检测相应阶段LECs的细胞周期情况。结果bFGF蛋白在LECs的原代、传第1、2代中明显表达,在传第3、4代中表达较弱。这与流式细胞法检测的细胞周期中有丝分裂相所占比例相符。结论bFGF参与LECs的增殖分化过程;并随着传代的递增,其促LECs增殖作用减弱,提示它与临床儿童后发性白内障发生率高有关。