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Objective:To investigate the impact of beta-elemene injection on the growth and alpha-tubule of human hepatocarcinoma HepG2 cells.Methods:Cell proliferation was assessed by MTT assay.Cell cycle distribution was detected by flow cytometry(FCM).The mRNA expression of alpha-tubulin was measured by RT-PCR.Western blot analysis was used to determine protein expression of alpha-tubulin and the polymerization of tubulin.Results:Beta-elemene injection inhibited HepG2 cells proliferation in a dose-and time-dependent manner;FCM analysis indicated beta-elemene injection induced cell cycle arrested at S phase.RT-PCR and westernblot analysis showed that beta-elemene injection down-regulated alpha-tublin at both mRNA and protein levels,presenting a dose-dependent manner.Moreover,beta-elemene injection reduced the polymerization of microtubules in a dose-dependent manner.Conclusions:Beta-elemene injection can inhibit the proliferation of hepatoma HepG2 cells and induce cell apoptosis,the mechanism might be partly related to the down-regulation of alpha-tubulin and inhibition of microtubular polymerization.
Objective: To investigate the impact of beta-elemene injection on the growth and alpha-tubule of human hepatocarcinoma HepG2 cells. Methods: Cell proliferation was assessed by MTT assay. Cell cycle was detected by flow cytometry (FCM). The mRNA expression of alpha-tubulin was measured by RT-PCR. Western blot analysis was used to determine protein expression of alpha-tubulin and the polymerization of tubulin. Results: Beta-elemene injection inhibited HepG2 cells proliferation in a dose- and time-dependent manner; FCM analysis indicated beta-elemene injection induced cell cycle arrested at S phase. RT-PCR and westernblot analysis showed that beta-elemene injection down-regulated alpha-tubulin at both mRNA and protein levels, presenting a dose-dependent manner. Moreover, beta- elemene injection reduced the polymerization of microtubules in a dose-dependent manner. Conclusions: Beta-elemene injection can inhibit the proliferation of hepatoma HepG2 cells and induce cell apoptosis, the mechanism mi ght be partly related to the down-regulation of alpha-tubulin and inhibition of microtubular polymerization.