动物实验,急性青光眼 z-bo 2020-09-01 401

　　Recently, researchers in China and the United States discovered that acute glaucoma in mice is an inflammatory disease. Increased intraocular pressure or inflammation leads to blindness. This work was published in PNAS magazine. PNAS has very important clinical significance in the treatment of so-called acute angle-closure glaucoma. This is the first study to clarify the inflammatory mechanism of blindness in acute glaucoma patients caused by elevated intraocular pressure.

　　Glaucoma refers to a common and difficult eye disease in which intraocular pressure rises intermittently or continuously. Glaucoma is one of the three main blindness diseases that cause blindness in humans. It is divided into acute and chronic glaucoma according to the anterior horn of the anterior chamber and the severity of its attack. Acute angle-closure glaucoma is an often painful emergency eye disease. The patient's intraocular pressure suddenly rises and directly leads to visual impairment. In this study, the researchers found that the rapid and continuous increase in intraocular pressure in mice turned on the gene (TLR4), which caused the activation of the caspase-8 protein. In turn, this signal protein causes the production of inflammatory proteins, which usually help mammals resist microbial infections.

　　Immune response is a double-edged sword. Under normal circumstances, inflammatory proteins that fight microbial infections can protect us from infection, but in acute glaucoma, the inflammatory response can stimulate retinal cell apoptosis (programmed cell death). To further confirm the inflammatory mechanism of high intraocular pressure and retinal damage, the researchers found that inhibiting the TLR4 gene or caspace-8 protein can delay the death of retinal cells in acute glaucoma mice.