动物造模,周期性麻痹模型 z-bio 2022-11-23 265

　　Objective: To establish and evaluate the model of hyperthyroid hypokalemic periodic paralysis in CaV1.1-R528H mice.

　　Methods: Thirty six 8-week-old CaV1.1-R528H male mice and 36 8-week-old wild type C57BL/6J male mice were used, respectively × two × The factorial design method was based on the principle of random weight (three factors were mutation, thyroxine and insulin factors, and two levels were with or without), which were divided into eight groups. Among them, the mice in the thyroxine treatment group were prepared with hyperthyroxine poisoning according to 350 μ L-thyroxine sodium was injected intraperitoneally for 12 days at the weight of g/kg. After the last administration, the insulin treated group was injected intraperitoneally with short acting insulin at the weight of 0.8 U/kg. The blood potassium of mice in each group before (0 min) and after (30, 60 min) injection was detected and recorded respectively.

　　Results: (1) The mice with hyperthyroxine poisoning developed restlessness, irritability and dull hair color. Compared with the control group, the amount of food and water increased significantly, but the weight increased slowly. Thyroid function test showed that T3 and T4 were significantly higher and TSH was significantly lower than the corresponding control group (P<0.05). (2) When treated with thyroxine or insulin alone, there was no statistical difference in blood potassium between the mutation group and the wild group at the same time point. However, after insulin treatment was given under hyperthyroidism, the blood potassium of the mutation group was significantly lower than that of the wild group at the same time point (30, 60 min) (P<0.05). (3) Main effect and interaction: single mutation factor or thyroxine factor has no effect on blood potassium, only insulin has effect on reducing blood potassium (P<0.05); There were interactions between thyroxine factor and mutation factor, and between insulin factor and mutation factor (P<0.05); There is no interaction between thyroxine factor and insulin factor.

　　Conclusion: (1) Hyperthyroxine poisoning was successfully prepared. (2) The model of hyperthyroid hypokalemic periodic paralysis was successfully established in CaV1.1-R528H mice by gene knockout.