动物造模,甲亢性低钾型周期性麻痹模型 z-bio 2021-09-17 354

　　Objective: To establish a hypokalemic hypokalemic periodic paralysis model with gene knock-in CaV1.1-R528H mice and evaluate it.

　　Methods: 8-week-old gene knock-in CaV1.1-R528H male mice and 8-week-old wild-type C57BL/6J male mice each were 36 mice, using a three-factor two-level 2×2×2 factorial design method according to the principle of weight randomization (The three factors are mutation, thyroxine and insulin, and the two levels are with or without) are divided into 8 groups. Among them, the mice in the thyroxine treatment group were prepared for hyperthyrotoxicosis, and levothyroxine sodium was continuously injected intraperitoneally at 350 μg/kg body weight for 12 days. After the last administration, the insulin treatment group was given intraperitoneal injection at 0.8 U/kg body weight. For effective insulin, the serum potassium levels before injection (0 min) and after injection (30, 60 min) were detected and recorded in each group of mice.

　　Results: (1) The mice prepared with hyperthyrotoxicosis showed irritability, irritability, and dry coat. Compared with the control group, the amount of diet and drinking water was significantly increased, and the weight gain was slow. 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, and the difference was significant (P<0.05). (2) When treated with thyroxine or insulin alone, there was no statistical difference in serum potassium between the mutant group and the wild group at the same time point. However, after insulin treatment under hyperthyroidism, the mutant group and the wild group were at the same time point ( 30 and 60 minutes) The serum potassium of the mutant group was significantly lower than that of the wild group (P<0.05). (3) Main effects and interactions: mutation factors alone or thyroxine factors have no effect on serum potassium, only insulin has an effect on reducing serum potassium (P<0.05); between thyroxine factors and mutation factors, and insulin factors and There was an interaction between the mutation factors (P<0.05); there was no interaction between the thyroxine factor and the insulin factor.

　　Conclusion: (1) The preparation of hyperthyrotoxicosis was successful. (2) The gene knock-in CaV1.1-R528H mice successfully established a hypokalemic hypokalemic periodic paralysis model.