寻找治疗GFS术后瘢痕形成更加安全、特异、有效的方法成为目前研究的难点。我们前期的研究发现：PPAR-γ在HTFs有确切的表达，而罗格列酮作为一种PPAR-γ激动剂可以拮抗TGF-β1诱导的HTFs活化，并且通过干预TGF-β/Smads信号通路特异性抑制GFS术后瘢痕形成。为改善罗格列酮的给药方式、延长其持续作用时间和最大限度降低其毒性作用，本研究拟以GFS术后瘢痕化的主要成份-HTFs异常增殖时细胞膜表面LDLr高表达为切入点，将LDL与罗格列酮结合形成复合体通过LDL-LDLr通路靶向性导入异常增殖的HTFs，在达到罗格列酮抗HTFs增殖作用的同时最大程度降低其毒性作用。同时引入壳聚糖海藻酸钙纳米微囊缓释技术，将LDL-罗格列酮复合体进行微囊化后进行缓释更好的对抗青光眼滤过术后的瘢痕化。这将为GFS术后抗瘢痕化的治疗提供一既提高罗格列酮生物利用度又降低毒副作用的新给药途径和新的方法。

Antifibrotic therapeutic methods with safety and effectiveness after glaucoma filtration surgery(GFS) are desirable.In the previous study using HumanTenon's Fibroblasts(HTFs) as a model,we have proved that peroxisome proliferator activates receptor-γ(PPAR-γ) expression is clearly in HTFs, rosiglitazone as an agonist of PPAR-γcan inhibit the reactivation of HTFs induced by transforming growth factorsβ1(TGF-β1), and rosiglitazone can inhibit specificly scarring after GFS with intervening TGF-β/Smads signal pathway.However the problems of further studies are what is the better drug delivery way of rosiglitazone and how to prolong the duration of rosiglitazone function and reduce the toxicity of rosiglitazone to ocular tissue. Based on the fact that LDLr is strongly expressed in HTFs proliferating abnormally after GFS,we structure targeting LDL- rosiglitazone complexes and channel them into HTFs accroding to LDL-LDLr pathway in order to promote anti-proliferation of HTFs and reduce the toxicity to ocular tissue.Meanwhile,in order to improve the release properties of LDL-rosiglitazone complexes,we structure release system of LDL-rosiglitazone-chitosan-calcium alginate(CCA)-microcapsules,which can be a new antifibrotic therapeutic methods on scarring after GFS and also a novelty administration of rosiglitazone.