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目的探讨氨氯地平对小鼠肝癌H22细胞的抑制作用及其机制。方法采用MTT法检测氨氯地平对小鼠肝癌H22细胞增殖的影响。建立肝癌H22荷瘤小鼠模型,观察氨氯地平对荷瘤小鼠肿瘤的抑瘤率;HE染色观察肿瘤组织的病理改变;免疫组织化学方法检测肿瘤组织中bcl-2和bax蛋白的表达水平。结果氨氯地平作用48h可显著抑制小鼠肝癌H22细胞增殖,且呈剂量依赖性,其半数抑制浓度为5.6×10-3mg/ml。体内试验显示,氨氯地平(3和10mg/kg·d)灌胃给药10d能显著抑制H22荷瘤小鼠肿瘤生长;HE染色可见,氨氯地平给药组小鼠肿瘤细胞核染色变浅,细胞排列紧密;免疫组化显示,氨氯地平给药组小鼠肿瘤组织内bcl-2蛋白表达下调,而bax蛋白表达上调。结论氨氯地平具有明显的抑瘤作用,其抑瘤机制可能与诱导肿瘤细胞凋亡相关。
Objective To investigate the inhibitory effect of amlodipine on mouse hepatoma H22 cells and its mechanism. Methods MTT assay was used to determine the effect of amlodipine on the proliferation of mouse hepatoma H22 cells. H22 tumor-bearing mice model of HCC was established to observe the tumor inhibition rate of amlodipine on tumor-bearing mice; the pathological changes of tumor tissues were observed by HE staining; the expression of bcl-2 and bax protein in tumor tissues was detected by immunohistochemistry . Results Amlodipine 48h inhibited the proliferation of H22 cells in a dose-dependent manner. The half inhibitory concentration was 5.6 × 10-3mg / ml. In vivo tests showed that amlodipine (3 and 10 mg / kg · d) administered orally for 10 days significantly inhibited the tumor growth in H22 tumor-bearing mice. HE staining showed that the staining of tumor cells in amlodipine-treated mice became lighter, Cells arranged closely; Immunohistochemistry showed that the expression of bcl-2 protein and bax protein were up-regulated in the tumor tissues of amlodipine-treated mice. Conclusion Amlodipine has significant anti-tumor effect, and its anti-tumor mechanism may be related to the induction of tumor cell apoptosis.