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后发性白内障的发病机制和药物防治的研究现状及前景

http://www.cnophol.com 2009-6-30 10:54:29 中华眼科在线

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    白内障摘出联合IOL植入术后,残留晶状体上皮细胞发生创伤愈合发应,并有巨噬细胞浸润且释放多种细胞因子。这些细胞因子在体内与其特异性受体结合,既可单独发挥作用,又可互相影响形成细胞因子网络,调节基因的转录以及细胞的生物学行为,从而引起后囊膜混浊。

    Nd:YAG激光囊膜切开可治疗后囊混浊的大多数病例[29-32]。但是即使手术后很长时间后囊中央保持透明,前部囊膜切开口边缘或后囊周边部的混浊阻碍眼底检查和光疗视网膜病变,所以希望能有安全、有效的药物治疗后发障。可能的治疗药物包括细胞毒药物、凋亡诱导剂或阻止细胞粘附的药物,但是它们同时对眼部的其他组织如视网膜、角膜内皮、小梁结构有伤害。为了减少眼内这些化学药物的扩散,最近有研究在人工晶状体表面包裹这些药物的缓释系统,如水凝胶。阻止上皮间质转化和细胞外基质的表达是防治后发障新的方向, TGFβ在这过程中起重要作用。CAT-152人单克隆抗TGFβ抗体是候选药物[33]。通过Smad3缺陷的大鼠的实验表明,表现为snail和α平滑肌肌动蛋白都不表达,所以切除Smad3信号完全阻止损伤诱导的晶状体上皮间质转化。腺病毒瞬时表达Smad7成功阻止组织纤维化反应[34,35],在晶状体损伤大鼠,腺病毒短期转移Smad7基因阻止上皮间质转化和抑制Smads2/3信号。

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