人参皂苷Rh2抗胶质瘤机制的研究进展

Advances in the mechanism of ginsenoside Rh2 against glioma

胶质细胞瘤是一种恶性程度极高的神经上皮组织肿瘤,目前已归入星形细胞瘤类别。其生长迅速,侵袭性强,预后极差。人参皂苷Rh2(GRh2)为类固醇化合物,能抑制胶质瘤细胞的生长与侵袭,并诱导胶质瘤细胞凋亡等,从而发挥抗癌作用。GRh2的抗肿瘤分子机制系通过抑制表皮生长因子受体(EGFR)/磷脂酰肌醇激酶(PI3K)/蛋白激酶B(Akt)/哺乳动物雷帕霉素靶蛋白(mTor)、c-Jun氨基末端激酶(JNK)、细胞外调节激酶(ERK)/丝裂原活化蛋白激酶(MAPK)信号通路,并且上调miRNA-128表达水平,抑制miRNA-21表达,从而抑制胶质瘤生长及促进其细胞凋亡,并可能下调基质金属蛋白酶(MMP)家族蛋白及血管内皮生长因子(VEGF)表达水平来减弱胶质瘤细胞侵袭性,可能调控核因子-κB(NF-κB)信号通路及免疫微环境的表达,以抑制促肿瘤因子的过度表达。该文对目前GRh2抗胶质瘤机制的研究进展作一综述。

Human glioblastoma multiforme is an extremely malignant neuroepithelial neoplasm characterized by rapid growth,high cell invasiveness and a poor prognosis.Currently,a variety of active molecules have been extracted from ginseng,of which ginsenoside Rh2(GRh2)is a steroid compound.Studies have shown this molecule exerts anti-cancer activities by inhibiting glioma cell growth and invasion,and inducing cell apoptosis and other anti-cancer biological behaviors.According to the literature,the evidence suggests GRh2 inhibits epidermal growth factor receptor(EGFR)/phosphatidylinositol kinase(PI3K)/protein kinase B(Akt)/mammalian target of rapamycin(mTor),c-Jun amino terminal kinase(JNK),extracellular regulation Kinase(ERK)/mitogen-activated protein kinase(MAPK)signaling pathways,increases microRNA-128(mi-RNA)expression levels and inhibits RNA-21 expression.,which inhibit glioma growth and promote apoptosis.Besides,GRh2 might decrease metalloproteinase(MMP)and vascular endothelial growth factor(VEGF)expression levels to weaken the invasion ability of glioma.It also might inhibit over-expression of protumor factors via regulating nuclear factor-κB(NF-κB)signaling pathway and immune microenvironments.This paper reviews the molecular mechanisms that underpin the GRh2 inhibitory role in glioma tissue,and provide references for further studies and clinical pharmacological experiments.