Chen Ying-Shan, Green Colin R, Wang Kailun, Danesh-Meyer Helen V, Rupenthal Ilva D
Department of Ophthalmology, University of Auckland, Auckland, New Zealand.
Department of Ophthalmology, University of Auckland, Auckland, New Zealand.
Eur J Pharm Biopharm. 2015 Sep;95(Pt B):378-86. doi: 10.1016/j.ejpb.2014.12.005. Epub 2014 Dec 9.
Recent research has shown that transient block of connexin43 (Cx43) hemichannels by mimetic peptides (MP) after retinal ischaemia inhibits uncontrolled hemichannel opening causing blood-brain barrier permeability and endothelial cell loss, and consequently provides improved retinal ganglion cell (RGC) survival. However, the highly hydrophilic character and potentially poor stability of native peptides can limit efficient delivery in a clinical setting. The present study investigated the ability of intravitreally injected Cx43 MP encapsulated into slow-release poly(lactic-co-glycolic) acid (PLGA) nano-(Nps) and microparticles (Mps) to promote RGC survival in a retinal ischaemia-reperfusion rat model. The particle size was around 113 nm (Nps) and 9 μm (Mps), respectively, with Cx43 MP entrapment efficiencies of 70% (Nps) and 97% (Mps). A triphasic in vitro release profile was observed with an initial burst of surface-bound Cx43 MP followed by slow release due to polymer erosion and further drug release at the point of complete particle breakdown, with 100% release achieved after 63 (Nps) and 112 (Mps) days, respectively. Nps showed the most promising results on both Cx43 down-regulation and RGC rescue in this acute injury model. Mps treatment, on the other hand, was unable to down regulate the initial inflammatory response possibly due to trapping of the bigger particles in the vitreous and the much slower release of Cx43 MP from these particles, but displayed a delayed effect on Cx43 regulation and RGC preservation due to the sustained release.
最近的研究表明,视网膜缺血后,模拟肽(MP)对连接蛋白43(Cx43)半通道的短暂阻断可抑制不受控制的半通道开放,从而避免血脑屏障通透性增加和内皮细胞丢失,进而提高视网膜神经节细胞(RGC)的存活率。然而,天然肽的高度亲水性和潜在的低稳定性可能会限制其在临床环境中的有效递送。本研究调查了封装在缓释聚乳酸-乙醇酸共聚物(PLGA)纳米颗粒(Nps)和微粒(Mps)中的玻璃体内注射Cx43 MP在视网膜缺血再灌注大鼠模型中促进RGC存活的能力。颗粒大小分别约为113 nm(Nps)和9 μm(Mps),Cx43 MP的包封率分别为70%(Nps)和97%(Mps)。观察到一种三相体外释放曲线,最初是表面结合的Cx43 MP的突发释放,随后由于聚合物侵蚀而缓慢释放,在颗粒完全分解时进一步释放药物,分别在63天(Nps)和112天(Mps)后实现100%释放。在这个急性损伤模型中,Nps在Cx43下调和RGC挽救方面显示出最有前景的结果。另一方面,Mps治疗无法下调初始炎症反应,这可能是由于较大颗粒被困在玻璃体内以及Cx43 MP从这些颗粒中释放得更慢,但由于持续释放,对Cx43调节和RGC保存显示出延迟效应。