Han Yong, Zhou Jing, Yu Shu-jing, Cui Bin, Zhang Hai-qing, Gao Ling, Zhao Jia-jun
Department of Endocrinology, Provincial Hospital Affiliated to Shandong University, Jinan, 250021, China.
Chin J Integr Med. 2009 Aug;15(4):284-8. doi: 10.1007/s11655-009-0284-8. Epub 2009 Aug 18.
To investigate the inhibitory effects of Kangjia Pill (KJP) on the cell proliferation in rat goiter model induced by methimazole (MMI).
Fifty-six Wistar rats were randomly divided into four groups: the normal group, MMI model group (MMI), low dose of KJP group (LKJP), and high dose of KJP (HKJP). Except the normal group (20 rats), the other groups (12 rats in each) were given 0.04% (w/v) MMI through the drinking water until the end of the experiment. One week later, the rats in the LKJP and HKJP groups were given KJP by gastrogavage at the dose of 250 mg/(kg x d) and 1,000 mg/(kg x d), respectively for 12 weeks. The relative thyroid weight (mg/100 g body weight) of each rat was accessed. The expression of proliferating cell nuclear antigen (PCNA) was determined by immunohistochemistry, and the correlation analysis between the PCNA positive thyrocytes and the relative thyroid weight was performed. The expressions of PCNA and cyclin D1 were examined with Western blotting.
After KJP treatment for 12 weeks, compared with the MMI group, the relative thyroid weight of the HKJP group decreased significantly, and the positive thyrocyte populations of PCNA in the two KJP groups reduced markedly (all P<0.05). The correlation analysis showed that PCNA was closely correlated with thyrocyte proliferation (r=0.685, P<0.05). KJP significantly decreased the protein expression of PCNA and cyclin D1 in the thyroid specimens (P<0.05), the high dose showed better effects.
KJP played a therapeutic role via inhibiting cell proliferation in the rat goitrous glands.
探讨甲亢丸（KJP）对甲巯咪唑（MMI）诱导的大鼠甲状腺肿模型细胞增殖的抑制作用。
56只Wistar大鼠随机分为四组：正常组、MMI模型组（MMI）、低剂量KJP组（LKJP）和高剂量KJP组（HKJP）。除正常组（20只大鼠）外，其他组（每组12只）通过饮用水给予0.04%（w/v）MMI直至实验结束。一周后，LKJP组和HKJP组大鼠分别以250mg/（kg·d）和1000mg/（kg·d）的剂量灌胃给予KJP，持续12周。测量每只大鼠的相对甲状腺重量（mg/100g体重）。采用免疫组织化学法检测增殖细胞核抗原（PCNA）的表达，并对PCNA阳性甲状腺细胞与相对甲状腺重量进行相关性分析。采用蛋白质印迹法检测PCNA和细胞周期蛋白D1的表达。
KJP治疗12周后，与MMI组相比，HKJP组的相对甲状腺重量显著降低，两个KJP组的PCNA阳性甲状腺细胞数量明显减少（均P<0.05）。相关性分析表明，PCNA与甲状腺细胞增殖密切相关（r=0.685，P<0.05）。KJP显著降低了甲状腺标本中PCNA和细胞周期蛋白D1的蛋白表达（P<0.05），高剂量组效果更佳。
KJP通过抑制大鼠甲状腺肿腺体中的细胞增殖发挥治疗作用。
