动物造模,甲亢性低钾型周期性麻痹模型 zi-bio 2024-03-06 578

　　Objective: To establish a hyperthyroidism hypokalemic periodic paralysis model in CaV1.1-R528H mice by knocking in genes and evaluate it.

　　Method: Thirty six 8-week-old CaV1.1-R528H male mice and thirty-six 8-week-old wild-type C57BL/6J male mice were randomly divided into eight groups based on weight randomization using a three factor, two level, 2x2x2 factorial design method (the three factors were mutations, thyroid hormone, and insulin factors, with or without two levels). Among them, mice in the thyroxine treated group were prepared for hyperthyroidism at a dose of 350 μ Continuous intraperitoneal injection of levothyroxine sodium at a dose of g/kg body weight for 12 days. After the last administration, the insulin treated group was given intraperitoneal injection of short acting insulin at a dose of 0.8 U/kg body weight. The blood potassium levels of each group of mice before injection (0 min) and after injection (30, 60 min) were measured and recorded.

　　Result: (1) Mice with high thyroxine toxicity showed restlessness, irritability, and dry fur. Compared with the control group, the diet and water intake increased significantly, while the weight gain was slow. The thyroid function test showed that T3 and T4 were significantly higher than the corresponding control group, and TSH was significantly lower than the corresponding control group, with significant differences (P<0.05). (2) When treated with thyroxine or insulin alone, there was no statistically significant difference in blood potassium between the mutant group and the wild group at the same time point. However, after insulin treatment under high thyroxine toxicity, the blood potassium in the mutant group was significantly lower than that in the wild group at the same time point (30 and 60 minutes) (P<0.05). (3) Main effects and interactions: Mutation factors alone or thyroid hormone factors have no effect on blood potassium, only insulin has an effect on reducing blood potassium (P<0.05); There are interactions between thyroid hormone factors and mutation factors, as well as between insulin factors and mutation factors (P<0.05); There is no interaction between thyroid hormone factors and insulin factors.

　　Conclusion: (1) The preparation of hyperthyroidism has been successful. (2) A hyperthyroidism hypokalemic periodic paralysis model was successfully established using gene knock-in in CaV1.1-R528H mice.