Glaucoma is one of the most common causes of irreversible
blindness. It is acknowledged that lowering intraocular pressure (IOP) is the effective treatment to slow
glaucoma disease progression. The main obstacle of existing drugs is that the effect of reducing IOP does not last long. Degradation of IκB stimulates the transcription of NF-κB, which could upregulate the expression of
matrix metalloproteinases (
MMPs). Whether a IκB-targeted gene therapy works in
glaucoma is unclear. Here, we established a chronic
ocular hypertension (COHT) model in rhesus monkey by
laser photocoagulation and verified that intracameral delivery of IκBα-
siRNA showed long-lasting and potent effects of reducing IOP without obvious
inflammation in monkeys with COHT. We also verified that IκBα-
siRNA could increase the expressions of MMP2 and MMP9 by knocking down IκBα in vitro and in vivo. Our results in nonhuman primates indicated that IκBα-
siRNA may become a promising therapeutic approach for the treatment of
glaucoma.