疾病动物模型,代谢性白内障动物模型 z-bio 2021-03-12 330

　　This type of cataract model uses a variety of drugs to affect the metabolism of the lens and form cataracts. Commonly used are D-galactose, sodium selenite, naphthalene, glucocorticoids, and the less frequently used bleomycin, pinomycin, bussuan and cysteamine. And xylazine and so on.

　　1, D-galactose-induced cataract animal model

　　[Modeling mechanism] Excessive D-galactose is metabolized in the lens to form galactitol. Galactitol cannot penetrate the lens capsule and accumulate in the lens, causing the lens to increase the osmotic pressure, leading to lens fibroedema, necrosis, and cataracts.

　　[Modeling method] According to the way you take galactose, it can be divided into three types.

　　(1) High galactose diet: Providing 50% to 60% galactose to weaned puppies can cause cataracts. There are some differences in the reproductive lineage. Generally, H (Holtzmann) rats are the shortest, followed by RW (Rochester Colony Wistar) rats and CN (Kerworth Farmneron) rats. Some people use guinea pigs instead of mice. Guinea pigs are close to the formation of galactosemic cataracts in the human body, because neither guinea pigs nor humans can synthesize vitamin C by themselves every day, and the antioxidant effect of vitamin C can delay the development of cataracts. Choose 300 g of adult guinea pigs fed a diet that does not contain vitamin C and contains 10% galactose, and the model usually forms within 9 days. (2) Intraperitoneal injection of galactose: intraperitoneal injection of 50% galactose solution (total 15-30 g/kg), 3 days after injection, small vesicles may appear in the equatorial region of the rat lens. The lens is completely muddy. When the injection volume exceeds 30 g/kg, all test mice will develop cataracts and complete lens opacity with the naked eye, but the mortality rate of test mice is higher. When the dose is lower than 15 g/kg, the disease develops later and the model becomes unstable.

　　(3) Retrobulbar galactose injection: use 0.2 ml of 0.4% galactose saline, once a day or twice a week, fix the eyeballs once each time, and inject them into guinea pigs. Cataract formation is very slow and can be controlled by two injections a week, and the boundaries between the various stages of cataract formation are clear. After the ball is injected 0 times a day, the lens will become completely cloudy quickly.

　　[Model Features] After feeding the galactose diet, the lens begins to become surrounding vesicles on the 4th day, and gradually expands to the center on the 7th day, and clearly enters the cortex in the vesicle phase on the 7th day and on the 10th day. cloudy. On the 14th day when the typical nuclear opacity begins, the main feature is the appearance of milky white turbidity in the center of the lens; on the 19th day, all the remaining animals enter the mature stage of cataracts, appearing milky white with visible reflections. The pupil is the naked eye and is the densest in the central area. About 30 days after the supply of galactose stopped, it began to reverse. After seeing a circular translucent area on the equator, the translucent area gradually spread to the center and became transparent. After 45 days, the cortical area became substantially transparent. Slit lamp inspection revealed linear turbidity scattered in the transparent area. Sixty days after the test, only the needle-shaped nucleus turbidity remained. [Model Evaluation and Application] In short, various methods of feeding galactose to experimental animals can induce cataracts. Among these methods, the high-galactose diet is the simplest method, but the results are slow and costly. Injecting the ball with a smaller amount of medicine will lead to faster results, but it will be more complicated to operate and will cause a big gap in your physiology. Intraperitoneal injection is not only low-dose, easy to operate, fast and close to physiological conditions, but also superior to oral and post-ball injection. However, the disadvantage of intraperitoneal injection of D-galactose is the high mortality of the model. The reason may be that D-galactose causes hypertonicity of abdominal tissues, dehydration of organs and tissue cells, dehydration of sodium, and organ dysfunction. The pathological process of galactose cataract formation is basically the same as that of diabetic cataract, and it is mainly used for the research of diabetic cataract.