细胞因子对青光眼滤过手术瘢痕化调控的研究进展

手术后瘢痕化是导致青光眼滤过手术失败的主要原因。多种细胞因子,如转化生长因子β（TGF-β）、血管内皮生长因子（VEGF）、结缔组织生长因子（CTGF）、白细胞介素（IL-1）和干扰素（INF）等参与青光眼滤过手术瘢痕化过程的调控。目前已研制出多种针对这些细胞因子的治疗性干预措施,在预防青光眼手术滤过通道瘢痕化方面具有很好的应用前景。本文对参与调控青光眼滤过手术瘢痕化的细胞因子以及针对性治疗措施进行综述。     

增殖性玻璃体视网膜病变发病的免疫机制

近年研究证实增殖性玻璃体视网膜病变（ＰＶＲ）中含有ＩｇＧ，ＩｇＡ、ＩｇＭ及补体Ｃ＿３等免疫大分子物质以及Ｔ淋巴细胞和巨噬细胞，并检测出多种细胞因子如白细胞介素及生长因子，还检测出Ｓ－抗原和细胞因子的ｍＲＮＡ。视网膜色素上皮细胞（ＲＰＥ）具有表现型转换、抗原提呈及多种分泌功能。我们认为，ＰＶＲ的免疫机制实质上是在分子和细胞生物学水平炎症和免疫功能细胞及其分泌的（以及血源性的）多种活性因子和多肽生长因子对眼内细胞增生的调控过程。其中ＲＰＥ细胞等增生的细胞也以内源性分泌方式参与自身的调控。     

增殖性玻璃体视网膜病变发病的免疫机制

近年研究证实增殖性玻璃体视网膜病变（ＰＶＲ）中含有ＩｇＧ、ＩｇＡ、ＩｇＭ及补体Ｃ３等免疫大分子物质以及Ｔ淋巴细胞和巨噬细胞，并检测出多种细胞因子如白细胞介素及生长因子，还检测出Ｓ－抗原和细胞因子的ｍＲＮＡ。视网膜色素上皮细胞（ＲＰＥ）具有表现转换、抗原提呈及多种分泌功能。我们认为，ＰＶＲ的免疫机制实质上是在分子和细胞生物学水平痰症和免疫功能细胞及其分泌的（以及血源性的）多种活性因子和多肽生长因子对     

晶体上皮细胞增生与细胞因子

本文综述了细胞因子在晶体上皮细胞增生中的作用。资料表明，某些细胞因子如转化生长因子，白细胞介素１、６，成纤维细胞生长因子，上皮生长因子等可促进晶体上皮细胞的增生和纤维化，而γ－干扰素则可能具有抗晶体上皮细胞增生的作用。认为对细胞因子的深入研究将有助于阐明后发障的形成机理，并为该病的防治开辟广阔的前景。     

晶体上皮细胞增生与细胞因子

本综述了细胞因了在晶体上皮细胞增生中的作用。资料表明，某些细胞因子如转化生长因子，白细胞介素１、６成纤维细胞生长因子，上皮生长因子等可促进晶体上皮细胞的增生和纤维化，而ｙ－干扰素则可能具有抗晶体上皮细胞增生的作用。     

糖尿病视网膜病变缺血再灌注损伤中相关调控因子的研究进展

糖尿病视网膜病变（DR）是一种常见的缺血性眼病。DR视网膜缺血再灌注（RIR）损伤的缺血过程、再灌注损伤过程及其结局3个阶段中氧化应激、钙超载、一氧化氮（NO）、兴奋性氨基酸（EAA）等因素引起多种炎性介质和基因过度表达,进而造成炎症反应、损伤、凋亡和坏死等组织改变和功能障碍。这些过程受凋亡基因、促红细胞生成素、单核细胞趋化蛋白1、血管内皮生长因子（VEGF）、碱性成纤维细胞生长因子（bFGF）、基质细胞衍生因子-1、NO、一氧化氮合酶（NOS）等多种相关因子的调控。就其中主要调控因子的特点及临床应用方面的研究进展进行综述。     

白内障超声乳化吸除术眼内液中细胞因子的改变

白内障超声乳化吸除术虽然相当微创,但仍会损伤血-眼屏障,导致眼内液中白细胞介素6(IL-6)、白细胞介素8(IL-8)、肿瘤坏死因子(TNF)、血管内皮生长因子(VEGF)、肝细胞生长因子(HGF)、单核细胞趋化蛋白-1(MCP-1)等多种促炎细胞因子升高,而色素上皮衍生因子(PEDF)、干扰素诱导蛋白(IP-10)、白细胞介素1β(IL-1β)、白细胞介素10(IL-10)等抗炎因子下降。这些变化可以引起或加重黄斑水肿、年龄相关性黄斑变性(AMD)、糖尿病视网膜病变(DR)等。研究眼内液中细胞因子的改变具有重要临床价值。     

白细胞介素-1、肿瘤坏死因子-α与眼病的关系研究进展

白细胞介素-1与肿瘤坏死因子-α是具有多种生物学效应的细胞因子.近年研究证实二者在角膜、视网膜等眼部多种组织中均有表达,且参与多种眼部疾病病理过程,如在干眼症患者中白细胞介素-1病理性升高,且参与慢性变应性结膜炎的发病,增生性糖尿病视网膜病变患者玻璃体和血清中二者含量均较正常人明显升高.用肿瘤坏死因子-α阻滞剂治疗葡萄...     

大鼠视网膜缺血再灌注后IL-1β的免疫组化研究

目的：观察大鼠视网膜缺血再灌注(retinal isehemia reperfusion，RIR)后，白细胞介素1β(IL-1β)多肽在视网膜表达变化。方法：采用前房灌注生理盐水，形成130mmHg(17．3kPa)高眼压，诱导大鼠视网膜缺血60min，解除高眼压，建立RIR模型。缺血60min，再灌注12h、48h作视网膜冰冻切片，IL-1β免疫组化观察。结果：正常对照组未见IL-1β表达，RIR后12h、48h，视网膜神经节细层可见IL-1β表达。结论：结果提示：IL-1β多肽在蛋白质水平参与RIR损伤发生。     

糖尿病视网膜病变发病机制相关因子的研究进展

糖尿病视网膜病变(DR)是最常见的视网膜血管病,其发生、发展受多种因素如细胞因子(血管内皮细胞生长因子、碱性成纤维细胞生长因子、胰岛素样生长因子-1、肝细胞生长因子、肿瘤坏死因子-α、转化生长因子-β、趋化因子、血小板源性生长因子-B)、黏附分子、肾素-血管紧张素系统、瘦素、内皮素、一氧化氮、糖基化终末产物、脂类代谢紊乱以栽及促红细胞生成素等的影响.就以上多种因素在DR的发生、发展中所起作用的研究进展进行综述.     

Growth factors: importance in wound healing and maintenance of transparency of the cornea

The mechanism of corneal wound healing has not been clarified yet. However, evidence has accumulated that various kinds of growth factor such as epidermal growth factor (EGF), fibroblast growth factor (FGF), transforming growth factor (TGF), keratinocyte growth factor (KGF), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF) and insulin-like growth factor (IGF) play a key role in corneal wound healing. For example, these growth factors are expressed in the corneal epithelial cells, keratocytes and endothelial cells, and their receptors are expressed in the corneal cells. Furthermore, these growth factors promote the proliferation of corneal cells and induce the migration of corneal cells. In addition to the growth factors, inflammatory cytokines such as interleukin (IL)-1, IL-6 and TNF-alpha are involved in corneal wound healing. These cytokines are expressed in the normal and inflammatory cornea after infections, alkaliburn, etc. where they control the growth of corneal cells and induce the migration of corneal cells. Thus, a number of growth factors and cytokines function in the regulation of corneal cell proliferation and in the maintenance of corneal transparency.     

Houttuynia cordata Thunb rescues retinal ganglion cells through inhibiting microglia activation in a rat model of retinal ischemia-reperfusion

AIM: To observe the melanin change of the retinal pigment epithelium (RPE) and choroid in the convalescent stage of Vogt-Koyanagi-Harada (VKH). METHODS: A retrospective study was performed on 40 eyes of 20 patients in the convalescent stage of VKH. Fundus photography (FP), multispectral imaging (MSI), and optical coherence tomography (OCT) were performed. RESULTS: In the VKH convalescent stage, focal RPE melanin accumulation (FRMA) was detected in 34 eyes (85%) on MSI and in 7 eyes (17.5%) on FP. FRMA was limited to the previous retinal detachment area in all 28 eyes (FRMA was detected in 34 eyes on MSI, which were enrolled, and 6 eyes lacked data in the acute stage). Sunset-glow fundus was detected in 20 eyes (50%) on FP. The mean density of FRMA in a 1-mm-diameter circular area of the fovea was 0.04±0.07 on MSI, which was significantly correlated with sunset-glow fundus (ρ=0.467, P=0.02). CONCLUSION: In the VKH convalescent stage, FRMA is derived from the RPE melanin change, and sunset-glow fundus is derived from the choroid melanin change. A higher density of FRMA in the fovea and sunset-glow fundus represents more serious depigmentation of melanin.     

细胞因子对视神经损伤修复作用的研究进展

创伤、代谢、高眼压等多种因素均可能造成视网膜神经节细胞和或视神经损伤，而视网膜神经节细胞损伤凋亡后无法自主再生，因此往往会造成视力下降甚至丧失等严重后果。对于视神经损伤，目前临床上尚无非常有效的治疗方法。近年有研究发现细胞因子可以明显促进视网膜神经节细胞的存活和轴突再生。本文就其中睫状神经营养因子、胶质源性神经营养因子、色素上皮衍生因子、粒细胞集落刺激因子、血浆凝血因子、促红细胞生成素等几种细胞因子促进视神经损伤修复作用的研究进展进行综述。     

CNTF, not other trophic factors, promotes axonal regeneration of axotomized retinal ganglion cells in adult hamsters

PURPOSE: To investigate the in vivo effects of trophic factors on the axonal regeneration of axotomized retinal ganglion cells in adult hamsters. METHODS: The left optic nerve was transected intracranially or intraorbitally, and a peripheral nerve graft was apposed or sutured to the axotomized optic nerve to enhance regeneration. Trophic factors were applied intravitreally every 5 days. Animals were allowed to survive for 3 or 4 weeks. Regenerating retinal ganglion cells (RGCs) were labeled by applying the dye Fluoro-Gold to the distal end of the peripheral nerve graft 3 days before the animals were killed. RESULTS: Intravitreal application of ciliary neurotrophic factor substantially enhanced the regeneration of damaged axons into a sciatic nerve graft in both experimental conditions (intracranial and intraorbital optic nerve transections) but did not increase the survival of distally axotomized RGCs. Basic fibroblast growth factor and neurotrophins such as nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3, and neurotrophin-4/5 failed to enhance axonal regeneration of distally axotomized RGCs. CONCLUSIONS: Neurons of the adult central nervous system can regenerate in response to trophic supply after injury, and ciliary neurotrophic factor is at least one of the trophic factors that can promote axonal regeneration of axotomized RGCs.     

Induction of interleukin-8 in human retinal pigment epithelial cells after denuding injury

AIM: To determine interleukin 8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) expression in response to mechanical injury in human retinal pigment epithelial (HRPE) cells. METHODS: Enzyme linked immunosorbent assay (ELISA) was performed to determine IL-8 and MCP-1 secretion by HRPE cells after mechanical denudation. IL-8 and MCP-1 mRNA expression by HRPE cells was assessed using semiquantitative RT-PCR. The effects of immunosuppressive drugs, dexamethasone (DEX) and cyclosporin A (CSA), as well as immunosuppressive cytokines, interleukin 4 (IL-4), interleukin 10 (IL-10), and interleukin 13 (IL-13), on chemokine expression in HRPE cells after denuding injury were analysed. RESULTS: Mechanical injury induced HRPE IL-8 mRNA and IL-8 secretion. Although MCP-1 mRNA was enhanced slightly after denuding injury, MCP-1 secretion was not increased. DEX and CSA inhibited HRPE chemokine expression after injury. IL-4 and IL-13 enhanced IL-8 and MCP-1 production by HRPE cells after injury while IL-10 had no effect. CONCLUSIONS: These results suggest that IL-8 may be involved in retinal inflammatory responses to injury and that DEX and/or CSA treatment may help control the inflammatory components of retinal diseases such as proliferative vitreoretinopathy.     

视网膜神经细胞生长发育中相关诱导因素的研究进展

视网膜神经细胞在生长发育过程中受多种因素影响，涉及神经细胞间、神经细胞与基质间、神经细胞和细胞外因子之间作用的复杂过程。脑源性神经营养因子和胶质细胞源性神经营养因子等神经营养因子在神经细胞发育中能够促进细胞存活和增殖，保护神经细胞功能；成纤维细胞生长因子和血小板源性生长因子等细胞因子对细胞生长有直接或间接作用，介导和调节细胞的生物学效应，改变微环境平衡，对视网膜神经细胞生长、分化和凋亡有着促进或抑制作用。[眼科新进展2007；27（2）：146—149]     

Neurotrophic Factors, Cytokines and Stress Increase Expression of Basic Fibroblast Growth Factor in Retinal Pigmented Epithelial Cells

Basic fibroblast growth factor (bFGF) and FGF receptors have been localized to photoreceptors and retinal pigmented epithelium (RPE), but the function of bFGF in adult retina and RPE is unknown. Exogenous bFGF has a neuroprotective effect in retina and brain and its expression is increased in some neurons in response to cytokines or stress. In this study, we investigated the effect of light, other types of stress, neurotrophic factors, and cytokines on bFGF levels in cultured human RPE.Some agents that protect photoreceptors from the damaging effects of constant light, including brain-derived neurotrophic factor (BDNF), ciliary neurotrophic factor, and interleukin-1β, increase bFGF mRNA levels in RPE cells. Intense light and exposure to oxidizing agents also increase bFGF mRNA levels in RPE cells and cycloheximide blocks the increase. An increase in bFGF protein levels was demonstrated by ELISA in RPE cell supernatants after incubation with BDNF or exposure to intense light or oxidizing agents. These data indicate that bFGF is modulated in RPE cells by stress and by agents that provide protection from stress and support the hypothesis that bFGF functions as a survival factor in the outer retina.     

Nerve growth factor effect on human primary fibroblastic-keratocytes: possible mechanism during corneal healing

In response to corneal injury, cytokines and growth factors play a crucial role by influencing epithelial-stromal interaction during the healing and reparative processes which may resolve in tissue remodeling and fibrosis. While transforming growth factor-beta1 (TGF-beta1) is considered the main profibrogenic modulator of these process, recently the nerve growth factor (NGF) appears as a pleiotropic modulator of wound-healing and inflammatory responses. Interestingly in the cornea, where NGF, trkA(NGFR) and p75(NTR) are expressed by epithelial cells and keratocytes, the NGF eye-drop induces the healing of neurotrophic or autoimmune corneal ulcers. During corneal healing, quiescent keratocytes are replaced by active fibroblast-like keratocytes/myofibroblasts. While the NGF effect on epithelial cells has been investigated, no data are reported for NGF effects on fibroblastic-keratocytes, during corneal healing. NGF, trkA(NGFR) and p75(NTR) were found expressed by fibroblastic-keratocytes. NGF was able to induce fibroblastic-keratocyte differentiation into myofibroblasts, migration, Metalloproteinase-9 expression/activity and contraction of a 3D collagen gel, without affecting their proliferation and collagen production. These data also show a two-directional control of fibroblastic-keratocytes by NGF and TGF-beta1. To sum up, the findings of this study indicate that NGF can modulate some functional activities of fibroblastic-keratocytes, thus substantiating the healing effects of NGF on corneal wound-healing.