Pengaruh Ekstrak Etanol Daun Murbei (Morus Alba L.) dengan Glibenklamid Terhadap Ekspresi Gen CYP3A4 pada Kultur Sel HepG2

Mulberry leaf is a traditional herb and predicted has ecdysteronecompound which act as antihyperglicemid. Glybenclamide is a synthetic medicine used to cure diabetes mellitus type 2. The leaf reported as competitive inhibitor of CYP3A4 enzyme, which metabolizingglibenclamide. However, in many cases, combination of herbs with synthesis drugs causes interaction if used at the same time. This research aimed to see interaction of ethanol mulberry leaf extract with glibenclamide through CYP3A4 gene expression in HepG2 cell culture.Sample of mulberry extract, glibenclamide, and combination both sample were tested into cell HepG2 culture. Then RNA were isolated and purification using real time PCR to see the gene CYP3A4 expression. As a result, mulberry extract acts as inhibitor enzyme CYP3A4, while glibenclamide is enzyme substrate.The combination of mulberry and glibenclamide showed increased of expression of CYP3A4 gene, means greater enzyme produced, and lower medicine on blood plasma.

Ethanol Extract of Root of Prunus persica Inhibited the Growth of Liver Cancer Cell HepG2 by Inducing Cell Cycle Arrest and Migration Suppression

Liver cancer is the second most lethal cancer and hepatocellular carcinoma (HCC) is the primary cancer subgroup. However, the current chemotherapy agents remain ineffective and present wide side effects for advanced HCC patient. In this study, we investigated the antitumor role of ethanol extract of root of peach tree (Prunus persica (L.) Batsch and hereafter designated as TSG in short of its Chinese name), which is an important ingredient in Chinese medicine prescription, in liver cancer cell HepG2. By cell viability assay, we showed that addition of TSG in the culture medium inhibited the cell growth of HepG2 cells in a dose and time-dependent way. Cell cycle analysis indicated that TSG caused sustained M/G2 phase arrest. The expression of mitosis-related protein Cdc25c was impaired upon TSG treatment. Furthermore, wound healing assay demonstrated that TSG treatment notably suppressed the migration of HepG2 cells and the expression of extracellular matrix metalloprotease, MMP3 and MMP9. Most significantly, administration of TSG inhibited in vivo tumor growth in nude mice. Our findings suggested that TSG may serve as a source to isolate anti-HCC therapeutic ingredients.