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目的:探讨加减玉女煎抗实验性甲状腺功能亢进症的作用及其相关机制。方法:小鼠每天皮下注射左旋甲状腺素钠350μg.kg-1造模,随机分为模型组、加减玉女煎颗粒2.17,4.33,8.66 g.kg-1不同剂量组,阳性对照他巴唑0.01 g.kg-1组,另设正常组。观察动物体重、心脏质量指数、心率、自发活动、耗氧量;R IA法测定血清T3,T4含量,放射强度测定法分析甲状腺吸碘率的变化。结果:与正常组比较模型组动物体重增长明显减慢,心率加快,心脏质量指数、自发活动次数、耗氧量增加(P<0.05);与模型组比较,加减玉女煎中、高剂量组及他巴唑组体重增长明显加快(P<0.05);心脏质量指数明显降低(P<0.05);自发活动次数明显减少(P<0.05),耗氧量明显降低(P<0.05)。模型组的心率(794.5±47.8)次/m in,较正常组(682.5±116.4)次/m in明显增加(P<0.05),低、中、高剂量组心率分别为(736.9±66.6),(742.1±62.3),(715.8±102.8)次/m in,与模型组比较明显减慢(P<0.05)。血清T3,T4含量模型组分别为(3.85±0.96),(234.46±58.11)μg.L-1,较正常组(0.99±0.30),(65.94±13.94)μg.L-1明显增加,加减玉女煎中剂量组血清T3,T4含量分别为(2.57±0.81),(164.27±72.63)μg.L-1;高剂量组为(2.70±0.55),(157.26±35.03)μg.L-1;他巴唑组(2.88±0.59),(172.65±39.73)μg.L-1均较模型组明显降低(P<0.01)。他巴唑有显著降低甲状腺吸125I率的作用(P<0.01),提示可拮抗甲状腺激素合成;加减玉女煎此作用较弱,无显著性差异。结论:加减玉女煎具有抑制实验性甲状腺功能亢进症的作用,其作用机制可能主要不是抑制甲状腺素合成而与拮抗甲状腺激素的作用或其他因素有关。
Objective: To investigate the effect of adding and subtracting Yushe decoction on experimental hyperthyroidism and its related mechanism. METHODS: Mice were injected daily with subcutaneous injection of levothyroxine sodium 350 μg.kg-1, and randomly divided into model group, addition and subtraction of 2.75 mg/kg, 1.36 g.kg-1 different dose groups, and positive control tatabine 0.01. G.kg-1 group, another normal group. Animal body weight, heart quality index, heart rate, spontaneous activity, and oxygen consumption were measured. Serum T3 and T4 levels were determined by RIA method, and changes in thyroid iodine uptake rate were analyzed by radiation intensity assay. RESULTS: Compared with the normal group, the body weight of the model group significantly decreased, the heart rate increased, the heart quality index, the number of spontaneous activities, and the oxygen consumption increased (P<0.05). Compared with the model group, the addition and subtraction of the high-dose group of the Yushu fried group The weight gain of the thiazide group was significantly increased (P<0.05); the heart quality index was significantly decreased (P<0.05); the number of spontaneous activities was significantly reduced (P<0.05), and oxygen consumption was significantly decreased (P<0.05). The heart rate of the model group was (794.5±47.8) times/m in, which was significantly higher than that of the normal group (682.5±116.4) times/m in (P<0.05). The heart rate of the low, middle and high dose groups was (736.9±66.6). (742.1±62.3), (715.8±102.8) times/m in, significantly slowed down compared with the model group (P<0.05). The levels of serum T3 and T4 in the model group were (3.85±0.96) and (234.46±58.11) μg.L-1, which were significantly higher than the normal group (0.99±0.30) and (65.94±13.94) μg.L-1. The contents of serum T3 and T4 in the medium-dose group were (2.57 ± 0.81) and (164.27 ± 72.63) μg. L-1, respectively. The high-dose group was (2.70 ± 0.55) and (157.26 ± 35.03) μg. L-1. Compared with the model group, the Tamiazole group (2.88±0.59) and (172.65±39.73)μg.L-1 were significantly lower (P<0.01). Tropizole significantly reduced the thyroid uptake rate of 125I (P<0.01), suggesting that it could antagonize thyroid hormone synthesis; addition and subtraction of jade and female decoction had weaker effect and no significant difference. Conclusion: The addition and subtraction of Yushujian can inhibit the experimental hyperthyroidism. Its mechanism of action may not be related to the inhibition of thyroid hormone synthesis but related to the antagonism of thyroid hormone or other factors.