摘要
目的探讨HMG-CoA还原酶抑制剂普伐他汀在体内抑制肝细胞癌增殖和侵犯的作用及其机制。方法建立HepG2细胞裸小鼠皮下移植瘤模型,腹腔注射浓度为5 mg/ml的普伐他汀,每只10 ml.kg-1.d-1。观察肿瘤的生长情况,实验结束时切取肿瘤称重,检测血中AFP水平。采用RT-PCR方法检测肿瘤组织MMMP-2和MMP-9的表达。结果普伐他汀抑制裸小鼠皮下移植型肝癌的生长,抑瘤率34.6%,普伐他汀组和对照组瘤重分别是(0.246±0.129)g和(0.376±0.102)g,差异有统计学意义(P<0.05);AFP表达分别为(2.657±1.465)μg/L和(4.206±1.204)μg/L,差异有统计学意义(P<0.05);MMP-9mRNA分别为(0.474±0.045)和(0.546±0.054),差异有统计学意义(P=0.01)。结论普伐他汀能抑制肝癌细胞的增殖,其机制主要是抑制MMP-9的表达。
Objective To investigate possible mechanism of pravastatin on the proliferation and invasion of human hepatocellular carcinoma in vivo. Methods The model of subcutaneously transplanted HCC was established in nude mice to study the antitumor effects of pravastatin. The expression of MMP-2 and MMP-9 was detected by RT-PCR. Results The mean tumor volum and weight in nude mice treated with pravastatin were significantly lower than those of the control group. The weight of tumors in pravastatin group was remarkably less than that of control group （0. 246 ± 0. 129） g and （0. 376 ± 0. 102） g （ P 〈 0.05 ）. The inhibition rate of tumor was 34.6%. The assay showed lower values of AFP in pravastatin group （ 2. 657 ± 1. 465 ）μg/L and （4. 206 ± 1. 204 ） μg/L （ P 〈 0.05 ）. MMP-9mRNA in pravastatin group was significantly lower than that of control group （ 0. 474 ± 0. 045 ） and （ 0. 546 ± 0. 054 ）, （ P = 0.01 ）. Conclusion Pravastatin can inhibit proliferation and invasion of HepG2 cells in vivo, the mechanism of which may be related to the inhibition of MMP-9.
出处
《广西医学》
CAS
2009年第2期166-168,共3页
Guangxi Medical Journal
关键词
肝细胞癌
普伐他汀
基质金属蛋白酶
Carcinoma
Hepatocellular
Pravastatin
Metalloproteinase
