动物造模,药效评价,病毒性心肌炎 z-bio 2024-07-29 514

    Selenium was discovered over 180 years ago, initially for its toxic effects on the liver. Later, it was found that selenium is essential for the growth of animals and humans at low concentrations, and toxic at high concentrations. It was confirmed as an essential trace element for animals and humans in 1957 and 1973, respectively. Within an appropriate concentration range, selenium has a wide range of effects such as antioxidant, anti infective, anti-tumor, maintaining cell membrane stability, and normal immune function in the body. Selenium deficiency can cause various diseases, and a large number of animal experiments have shown that selenium deficiency can damage the immune system function, alter the virulence of viruses, and enhance the susceptibility of myocardial cells to viruses.

　　1. Pathogen Coxsackievirus Bh (CVB3m), its TCD50 was measured on Hela cells to the power of 10-7, with a dosage of 1000TCD50/0.1ml per experiment.

　　2. Animals should be fed with low selenium and high selenium synthetic feed to male BALB/c mice at 5 weeks of age for 5 weeks.

　　3. Infection route: Intraperitoneal injection of 0.1ml of 1000 TCD50 virus.

　　4. Pathological manifestations: Under light microscopy, it can be seen that 7 days after infection with CVB3m in the low selenium virus group, myocardial cells undergo degeneration and necrosis, muscle fibers dissolve and disappear, inflammatory cells infiltrate, and scattered focal necrosis and inflammatory lesions are formed. The lesions are mostly located in the middle layer of the left ventricular wall. Brown brown apoptotic cells can be seen in the myocardium of low selenium virus mice, with apoptotic cells accounting for 55% to 75% of the mice, mainly scattered around myocardial necrosis lesions or subepicardial myocardium.

　　5. Advantages and disadvantages: This model suggests that low selenium can promote myocardial cell apoptosis caused by viral infection, which can be used to explore the relationship between low selenium viral myocarditis and myocardial apoptosis.