Long-acting sustained release preparation for preventing or treating retinal damage, and preparation method thereof

Abstract

The invention belongs to the field of pharmaceutical preparations, and relates to a long-acting sustained release preparation for preventing or treating retinal damage, and a preparation method thereof. The long-acting sustained release preparation takes erythropoietin (EPO) as an active component, takes dextran as a protective agent for the active component, and takes poly(lactic-co-glycolic acid), polylactic acid or polycaprolactone as a coating component to prepare sustained release microspheres, wherein the erythropoietin is coated by the poly(lactic-co-glycolic acid), polylactic acid or polycaprolactone. Proven by animal experiments, the sustained release microspheres of the long-acting sustained release preparation provided by the invention have the same protective actions on the ganglionic cells of damaged retinas by single vitreous chamber injection and repeated EPO protein vitreous chamber injection, and the sustained release microspheres are capable of avoiding a series of complications caused by many times of injection and overcoming the defects of repeated intraocular injection administration and gene therapy. The long-acting sustained release preparation provided by the invention adopts intraocular local administration, can reduce the dosage and treatment cost, and can not generate adverse effects on other organs or tissues in vivo.

Description

technical field

[0001] The invention belongs to the field of pharmaceutical preparations, and relates to a long-acting slow-release preparation for preventing or treating retinal damage and a preparation method thereof. Background technique

[0002] It has been reported in the literature that there are various types of retinal optic nerve diseases, which are one of the important blinding factors. At present, there is no effective treatment method in ophthalmology clinic. Studies have shown that after the optic nerve is injured, the axon of retinal ganglion cells is damaged, resulting in the blockage of axoplasmic transport at the cribriform plate of the axons, resulting in insufficient supply of neurotrophic factors, release of excitatory neurotransmitters, oxidative stress and A large number of free radicals are produced, affecting the normal function of retinal ganglion cells (RGCs), causing their degeneration and death; the toxic media produced by the death of retinal gan...

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