人参皂苷Rg3调控ERK通路抑制Lewis小鼠肺癌生长的研究

Ginsenoside Rg3 inhibitions Lewis lung carcinoma growth by mediating ERK pathway

目的:通过人参皂苷Rg3对Lewis肺癌小鼠模型及其细胞模型的抑制研究,探讨ERK信号通路及相关基因在抗肿瘤中的作用。方法:建立Lewis肺癌小鼠荷瘤动物模型,通过口饲法给予定量人参皂苷,连续3周,处死动物后,比较各组荷瘤小鼠肿瘤体积。含药动物血清作用于Lewis肺癌细胞,MTT法检测各组细胞抑制效率。Realtime-PCR法检测荷瘤鼠Dusp6、Bax、Bcl-2基因表达变化,Western blot法检测荷瘤鼠ERK、p-ERK蛋白表达变化。结果:人参皂苷Rg3对Lewis肺癌细胞及荷瘤小鼠的肿瘤生长均有明显抑制作用(P<0.01)。Western blot显示ERK在Rg3处理组中的表达明显比对照组低,Realtime-PCR结果显示,在动物肿瘤标本中,Dusp6、Bax基因药物处理组比对照组高表达(P<0.01),Bcl-2基因药物处理组比对照组低表达(P<0.01)。结论:人参皂苷Rg3在Lewis肺癌体内外模型中具有一定的肿瘤抑制效果,ERK信号通路及Dusp6基因与Rg3的抑制作用有关,Rg3诱导的细胞凋亡也参与了抗肿瘤的作用。

Objective： To discuss the ERK pathway and its relative genetic function in Lewis lung carcinoma animal and cell model through Ginsenoside Rg3 treatment. Methods： The Lewis lung carcinoma mice model was established, After feeding Rg3 by gavage for 3 weeks, then the volumes of the tumor were calculated. The inhibition effect on Lewis lung carcinoma cell line was detected by MTT assay. The changes in Dusp6, Bax, Bcl-2 expressions in tumor model were detected by Reahime-PCR.The changes in ERK and p-ERK protein expression were determined by Western blot. Results： Ginsenoside Rg3 could inhibit Lewis lung carcinoma cell and animal model （P〈0.01）. ERK protein expression was significantly decreased in Rg3 group compared with control group by Western blot assay. Dusp6 and Bax were over expressed in Rg3 group compared with control （P 〈0.01） while the Bcl-2 was under expressed（P〈0.01）. Conclusion： Ginsenoside Rg3 exhibits certain inhibition ability in both in vivo and in vitro model. ERK pathway and Dusp6 gene are associated with the Rg3 inhibition effect, and the apoptosis effect induced by Rg3 is also involved in the inhibition.