The efficacy and safety of intravitreal conbercept combined with mitomycin C augmented trabeculectomy for treating neovascular glaucoma.

AIM: To investigate the efficacy and safety of intravitreal Conbercept (IVC) and trabeculectomy for treating neovascular glaucoma (NVG). METHODS: We retrospectively reviewed a total of 29 eyes from 29 NVG patients. All patients received preoperative IVC combined with mitomycin C (MMC) augmented trabeculectomy with a 12-month follow-up. The best-corrected visual acuities (BCVA), intraocular pressure (IOP), and cumulative survival rate were calculated. RESULTS: All 29 cases had complete regression of iris neovascularization at 7 days after the combination treatment, and 2 cases had residual iris neovascularization which regressed completely 1 month later. IOP decreased while BCVA improved significantly following the combination treatment. The success rates were 96.6%, 93.1%, 89.7%, 86.2%, and 82.8% at 1 week, 1, 3, 6, and 12 months after trabeculectomy, respectively. IVC injection combined trabeculectomy had few complications. CONCLUSIONS: IVC injection of conbercept combined with trabeculectomy is effective and safe for the treatment of NVG.

Caffeic acid phenethyl ester attenuates nuclear factor­κB­mediated inflammatory responses in Müller cells and protects against retinal ganglion cell death.

Glaucoma is characterized by the death of retinal ganglion cells (RGCs) and visual field defects, and is a leading cause of blindness worldwide. Caffeic acid phenethyl ester (CAPE), a natural polyphenolic found in propolis from honeybee hives, can inhibit the activation of nuclear factor κ light­chain­enhancer of activated B cells (NF­κB) and has therapeutic potential in inflammatory disease. The present study used a rat model of optic nerve crush (ONC) injury to investigate the effect of CAPE on glaucoma. The death of RGCs at day 14 was significantly reduced in CAPE­treated animals compared with the non­treated group according to Brn3a and TUNEL staining. In addition, CAPE decreased the severity of inflammation in the retina, reflected by the decreased expression of inflammatory cytokines, including interleukin (IL)­8, IL­6, inducible nitric oxide synthase, cycloooxygenase­2, tumor necrosis factor­α and chemokine C­C ligand­2, in CAPE­treated rats. The hypertrophy of astrocytes and Müller cells (gliosis) caused by ONC was also found to be attenuated by CAPE, accompanied by the inhibition of NF­κB signaling. Similarly, in vitro, CAPE suppressed the proliferation and migration of primary astrocytes induced by lipopolysaccharide, as well as the activation of NF­κB. These results suggest that CAPE protected against RGC and attenuated inflammatory responses in a rat model of ONC by suppressing NF­κB activation.