动物造模,急性青光眼 z-bio 2021-08-03 268

　　Recently, researchers in China and the United States have discovered that acute glaucoma in mice is mainly an inflammatory disease. Increased intraocular pressure or inflammation can cause vision loss.

　　This research was published in PNAS magazine. It has very important clinical significance for the treatment of so-called acute angle-closure glaucoma. This is the first time to clarify the inflammatory mechanism of vision loss in patients with acute glaucoma caused by high intraocular pressure.

　　Glaucoma refers to a common and difficult eye disease with intermittent or continuous increase in intraocular pressure. Glaucoma is one of the three major causes of blindness in humans. According to the anterior angle of the anterior chamber and the severity of the disease, it is divided into acute angle-closure glaucoma and chronic angle-closure glaucoma. Acute angle-closure glaucoma is usually a painful emergency ophthalmology. The patient's intraocular pressure suddenly rises, which directly damages vision.

　　In this study, the researchers found that the rapid, continuous and significant increase in intraocular pressure in mice turned on the gene (TLR4), which led to the activation of the caspase-8 protein. This signal protein usually produces inflammatory proteins that help mammals fight 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). For further confirmation

　　The relationship between high intraocular pressure and the inflammatory mechanism of retinal injury, researchers have found that inhibiting TLR4 gene or caspace-8 protein can delay the death of retinal cells in acute glaucoma mice.