Abstract
Glaucoma is associated with increased intraocular pressure (IOP), causing the apoptosis of retinal ganglion cells (RGCs) and the loss of their axons leading to blindness. Pituitary adenylate cyclase activating polypeptide (PACAP) is neuroprotective in several neural injuries, including retinopathies. The aim of this study was to investigate the effects of PACAP1-38 eye drops in a model of glaucoma. IOP was elevated bilaterally by injections of microbeads to block the aqueous humor outflow. The control groups received the same volume of saline. Animals were treated with PACAP1-38 (1 µg/drop, 3 × 1 drop/day) or vehicle for 4 weeks starting one day after the injections. Retinal morphology by histology and optical coherence tomography, function by electroretinography, and IOP changes were analyzed. Animals were sacrificed 8 weeks after the injections. Microbeads injections induced a significant increase in the IOP, while PACAP1-38 treatment lowered it to normal levels (~10 mmHg). Significant retinal degeneration and functional impairment were observed in the microbead-injected group without PACAP1-38 treatment. In the microbeads + PACAP1-38 group, the retinal morphology and functionality were close to the normal values. In summary, our results show that PACAP1-38, given in form of eye drops, is neuroprotective in glaucoma, providing the basis for potential future therapeutic administration.
Highlights
IntroductionThe most common form of it is open-angle glaucoma, which is a progressive condition that develops by the blockage of the aqueous humor (AH) drainage system leading to intraocular hypertension
Glaucoma refers to a group of optic neuropathies
In control situations (phosphate-buffered saline (PBS) + Systane (S) and PBS + PACAP138 (P)), we did not detect any changes in the intraocular pressure (IOP) (Figure 1A)
Summary
The most common form of it is open-angle glaucoma, which is a progressive condition that develops by the blockage of the aqueous humor (AH) drainage system leading to intraocular hypertension. The increased intraocular pressure will cause the loss of the RGCs and their axons [1]. Treatments are limited to moderate the intraocular pressure (IOP) elevation; retinal degeneration continues to progress at a slower rate. There is an emerging need for therapeutic agents that can prevent apoptosis and exert a neuroprotective effect [2]. The exact underlying mechanism of RGC apoptosis in glaucoma has not been fully clarified [3], evidence shows that oxidative stress, glial activation, and inflammatory reactions play a role in the pathomechanism [4,5,6,7]
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