小鼠急性青光眼 z-bo 2020-11-03 376

　　Recently, Chinese and American researchers have discovered that acute glaucoma in mice is largely an inflammatory disease. The increase in eye pressure or inflammation leads to vision loss.

　　This study was published in the journal PNAS, which has very important clinical significance for the treatment of so-called acute angle-closure glaucoma. The study is the first to reveal the inflammatory mechanism of vision loss in acute glaucoma patients caused by high intraocular pressure.

　　Glaucoma refers to a common and difficult eye disease in which intraocular pressure increases intermittently or continuously. Glaucoma is one of the three major blindness diseases that cause blindness in humans. According to the shape of the anterior chamber and the severity of onset, it is divided into acute and chronic angle-closure glaucoma. Acute angle-closure glaucoma is often a painful emergency ophthalmology, the patient has a sudden increase in intraocular pressure and direct visual impairment.

　　In this study, the researchers found that the rapid, sustained and large increase in intraocular pressure in mice turned on the gene (TLR4), which caused the activation of the caspase-8 protein. In turn, this signaling protein triggers the production of inflammatory proteins that normally help mammals fight microbial infections.

　　The immune response is a double-edged sword, because under normal circumstances, the inflammatory protein that fights microbial infections protects us from infection, but in the case of acute glaucoma, the inflammatory response stimulates the apoptosis of retinal cells (programmed Cell death).

　　In order to further confirm the relationship between high intraocular pressure and the inflammatory mechanism of retinal damage, the researchers found that inhibition of TLR4 gene or caspace-8 protein can slow down the death of retinal cells in acute glaucoma mice.