论文部分内容阅读
目的观察β-细辛醚对人胃癌MGC-803细胞BALB/c裸鼠皮下移植瘤上皮间质转化(epithelialmesenchymal transition,EMT)的影响并探讨其分子机制。方法将胃癌MGC-803细胞接种于裸鼠皮下制备移植瘤模型。随机分为阴性对照组(模型组)、阳性对照组(5-FU组,25 mg/kg)、β-细辛醚高剂量组(100mg/kg)、低剂量组(50 mg/kg),每组8只,各组灌胃给药,每日1次,连续用药10日。干预结束后处死小鼠,计算抑瘤率;通过实时定量PCR及Western Blot法检测移植瘤中EMT上皮型标志物E-钙黏蛋白(E-cadherin)、间质型标志物N-钙黏蛋白(N-cadherin)、转录因子Snail以及磷脂酰肌醇3-激酶(phosphatidylinositol3-kinase,PI3K)、磷酸化磷脂酰肌醇3-激酶(phosphorylation of phosphatidylinositol 3-kinase,p-PI3K)、丝氨酸-苏氨酸激酶(serine/threonine kinase,AKT)、磷酸化丝氨酸-苏氨酸激酶(phosphorylation of serine/threonine kinase,p-AKT)的表达。结果与模型组比较,5-FU组、β-细辛醚高、低剂量组第7~11日移植瘤体积明显缩小(P<0.05),N-cadherin、Snail、p-AKT、p-PI3K蛋白及m RNA表达降低(P<0.05),E-cadherin蛋白及m RNA表达升高(P<0.05)。结论β-细辛醚对胃癌细胞增殖能力有抑制作用,其机制可能与下调胃癌细胞的PI3K/AKT信号通路,抑制胃癌细胞EMT有关。
Objective To observe the effect of β-asarone on the epithelialmesenchymal transition (EMT) of human gastric cancer cell line MGC-803 and its molecular mechanism. Methods MGC-803 cells were inoculated subcutaneously in nude mice to prepare xenograft model. The rats were randomly divided into 5 groups: negative control group (model group), positive control group (25 mg / kg), β-asarone high dose group (100 mg / Each group of 8, each group intragastric administration, 1 day, continuous medication on the 10th. The mice were sacrificed after the intervention, and the tumor inhibition rate was calculated. The expression of EMT epithelial markers E-cadherin, interstitial markers N-cadherin in transplanted tumors were detected by real-time PCR and Western Blot. N-cadherin, Snail and phosphatidylinositol 3-kinase (PI3K), phosphorylation of phosphatidylinositol 3-kinase (p-PI3K), serine- Serine / threonine kinase (AKT) and phosphorylation of serine / threonine kinase (p-AKT). Results Compared with the model group, the tumor volume in the 5-FU group and the β-asarone high and low dose groups were significantly reduced (P <0.05), the expressions of N-cadherin, Snail, p-AKT and p-PI3K The protein and m RNA expression decreased (P <0.05), and the expression of E-cadherin protein and m RNA increased (P <0.05). Conclusion β-asarone can inhibit the proliferation of gastric cancer cells. The mechanism may be related to the down-regulation of PI3K / AKT signaling pathway and the inhibition of EMT in gastric cancer cells.