目的 通过观察海藻与甘草不同比例配伍的海藻玉壶汤对丙硫氧嘧啶造成的甲状腺肿大大鼠模型生物效应的影响,筛选出海藻与甘草配比起效的适宜条件,并对其作用机制进行初步探讨.方法 将海藻与甘草按照2因素7水平的均匀设计实验原则设置不同配伍比例的海藻玉壶汤,Wistar大鼠120只,随机分为10组,采用ig丙硫氧嘧啶14 d复制动物模型,造模后各组ig给药28 d,实验结束后测定大鼠甲状腺质量,测定血清中三碘甲腺原氨酸(T3)、四碘甲腺原氨酸(T4)、促甲状腺激素(TSH)等甲状腺激素水平,RT-PCR法测定大鼠甲状腺中甲状腺过氧化物酶(TPO)和甲状腺球蛋白(Tg)的mRNA表达.结果 海藻玉壶汤中海藻与甘草不同配比在不同程度上均有调节甲状腺激素水平、改善丙硫氧嘧啶所致的甲状腺肿大作用.与模型组比较,配比5组(0.135:8.32)较模型组TPO mRNA的表达显著升高.海藻玉壶汤配比1组(14.522:6.24)、5组、6组(29.040:4.16)的Tg mRNA水平较对照组显著升高.结论 海藻玉壶汤中海藻与甘草不同配比在不同程度上均能抑制丙硫氧嘧啶所导致的甲状腺肿大,以配比1组、3组(19.363:0.54)、6组表现最为明显,其作用机制可能涉及刺激TPO与Tg基因转录的增强.配比1组与配比5组具有促进这种代偿增强的作用,在某种程度上对甲状腺激素水平的恢复起到积极的作用.
Objective To explore the mechanism and compensation proceeding of Haizao Yuhu Decoction (HYD) with different compatibility of Sargassum and Glycyrrhizae Radix in goiter model rats caused by propylthiouraeil (PTU). Methods HYD with different compatibility of Sargassum and Glycyrrhizae Radix was set up according to the principle uniform design (two factors, seven levels), and 120 Wistar rats were randomly divided into 10 groups. PTU was ig given to rats for 14 d to establish the goiter model, and then the rats were ig administered with HYD for 28 d. All animals were sacrificed after the last dosage, the thyroid weight and changes of thyroid hormone levels of triiodothyronine (T3), thyroxine (T4), and thyroid stimulating hormone (TSH) in serum were determined, and the mRNA expression of thyroid peroxidase (TPO) and thyroglobulin (Tg) was detected by RT-PCR. Results HYD with different compatibility of Sargassum and Glycyrrhizae Radix could regulate thyroid hormone levels and inhibit thyroid enlargement induced by PTU in some degree. Compared with the model group, the TPO mRNA expression of group 5 (0.135 : 8.32) was significantly increased, and groups 1 (14.522 : 6.24), 5, and 6 (29.040 : 4.16) could also increase the Tg mRNA level significantly. Conclusion HYD with different compatibility could inhibit thyroid enlargement induced by PTU in some extent, the effects in groups 1 (14.522 : 6.24), 3 (19.363 : 0.54), and 6 (29.040 : 4.16) are the most obvious, and the mechanism may be related to the activation of gene transcription of TPO and Tg. The groups 1 and 5 could enhance the compensatory action to a certain degree.