The authors have manufactured a novel rabbit foldable capsular vitreous body (FCVB). The aim of this study was to determine whether this rabbit FCVB can release levofloxacin in vitro and in vivo, and to evaluate the release characteristics. In vitro, the rabbit FCVB with levofloxacin 500 μg/mL was immersed in cups of modified Franz diffusion cells. Following this, 200 μL of liquid was aspirated at intervals from 10 minutes to 24 hours. In vivo, the FCVB with levofloxacin was implanted into the right eyes of five rabbits. After implantation, the aqueous humor was aspirated on days 1, 7, 14, 28, and 56. The levofloxacin concentrations in the cups and aqueous humor samples were detected by high-performance liquid chromatography–tandem mass spectrometry. The FCVB was observed under a scanning electron microscope. The results showed that the released levofloxacin was stabilized at 20 ng/mL at time points from 10 minutes to 24 hours in vitro. In vivo, levofloxacin concentrations in the aqueous humor were 132, 50, 39, 11, and 15 ng/mL on days 1, 7, 14, 28, and 56, respectively. In the FCVB capsules, 300 nm apertures were observed. These results suggest the rabbit FCVB released levofloxacin stably in vitro and sustainably in vivo. This study provides a novel combined approach, with the FCVB as a vitreous substitute and drug delivery system for the treatment of bacterial endophthalmitis.
Aim:To evaluate the effects of small interference RNA protein kinase C-alpha (siRNA-PKCα) on experimental proliferative vitreoretinopathy (PVR) induced by dispase in mice. Methods: C57BL/6 mice PVR models (4-6 weeks old) were induced by intravitreal injection of dispase and then equally divided into six groups. After 1 week, the five treatment groups received 2 µL intravitreal injections of siRNA-PKCα at a concentration of 250 nM, 500 nM, 750 nM, 1000 nM, and 1500 nM, respectively, while the negative control group received 2 µL of 500 nM no-silencing siRNA. SiRNA-PKCα was transfected by a square wave electroporator. Postoperative ophthalmic observations of lens clarity and the fundus of the eyes were performed periodically. The eyeballs of the mice were enucleated and imbedded in optimal cutting temperature to perform histological and immunofluorescence analysis at the end of a 4-week observation period. Results: Four weeks after the siRNA-PKCα injections, there are 100% lens dissolution and 100% PVR in the 250 nM group and 70%, 70%, 70%, and 50% PVR in the 500 nM, 750 nM, 1000 nM, and 1500 nM groups, respectively, which is significantly different from the negative group. Abnormalities in fundus appearance were related to the concentrations of siRNA-PKCα; a higher concentration of siRNA-PKCα resulted in a more normal fundus. Histological sections by hematoxylin-eosin staining of the eyes support the clinical observation. Immunofluorescence analysis showed that RPE65, glutamine synthase, glial acidic fibrillary protein, and α-smooth muscle actin were increasing in the retina with the decreasing concentration of siRNA-PKCα, indicating that intraocular siRNA-PKCα can partly inhibit changes of markers for glia cells, fibroblast cells, retinal pigment epithelium cells, and Müller cells in the process of PVR. Conclusion: Gene therapy with siRNA-PKCα could effectively inhibit PVR in mice and provide us with a novel therapeutic target on PVR.
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