The effect of beta-elemene on alpha-tubulin polymerization in human hepatoma HepG2 cells

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 western- blot 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.

The impact of beta-elemene on beta-tubulin of human hepatoma hepg2 cells

Objective: The aim of this study was to investigate the impact of beta-elemene injection on the growth and beta-tubulin 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 beta-tubulin was measured by RT-PCR. Western blot analysis was used to determine protein expression of beta-tubulin and the polymerization of beta-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 western-blot analysis showed that beta-elemene injection down-regulated beta-tubulin expression 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. Conclusion: Beta-elemene injection can inhibit the proliferation of hepatoma HepG2 cells, the mechanism might be partly related to the down-regulation of beta-tubulin and inhibition of microtubular polymerization.

Downregulation effects of beta-elemene on the levels of plasma endotoxin,serum TNF-alpha,and hepatic CD14 expression in rats with liver fibrosis

It has been demonstrated thatβ-elemene could protect against carbon tetrachloride(CCl_(4))-induced liver fibrosis in our laboratory work,and the aim of this paper is to reveal the protective mechanisms ofβ-elemene.The hepatic fibrosis experimental model was induced by the hypodermical injection of CCl_(4) in Wistar male rats.β-elemene was intraperitoneally administered into rats for 8 weeks(0.1 mL/100 g bodyweight per day),and plasma endotoxin content was assayed by biochemistry.The serum TNF-αlevel was detected using radioactive immunity.CD14 expression in rat livers was measured by immunohistochemistry and Western blot.The results showed thatβ-elemene can downregulate the levels of plasma endotoxins,serum TNF-α,and hepatic CD14 expression in rats with liver fibrosis.β-elemene plays an important role in downregulating the lipopolysaccharide signal transduction pathway,a significant pathway in hepatic fibrosis development.

Influence ofβ-elemene on the secretion of angiotensin II and expression of AT1R in hepatic stellate cells

This study aims to investigate the influence ofβ-elemene on the secretion of angiotensin II(ANG II)and the expression of angiotensin receptor type 1(AT1R)in hepatic stellate cells(HSCs).In vitro,HSC-T6 were cultured for 24 hours and then treated with different doses ofβ-elemene(2.5,5 and 10 mg/L).A control group was also set up.The secretion of ANG II in the supernatant was detected by radioimmunoassay.The mRNA expression of AT1R at 4,12 and 24 h after treatment was detected by reverse transcription-polymerase chain reaction(RT-PCR),respectively.The protein expression of AT1R was detected by western blot.At the 4th h,the ANG II secretion in the supernatant was significantly inhibited by 10 mg/Lβ-elemene compared with the control group(P<0.05),while 5.0 mg/L and 2.5 mg/Lβ-elemene had no inhibitory effect on the secretion of ANG II(P>0.05).At the time point of the 12th h,the secretion of ANG II in the supernatant treated with 10 mg/L and 5.0 mg/Lβ-elemene was significantly lower than the control(P<0.01,P<0.05).Following the treatment with 5.0 mg/L and 2.5 mg/Lβ-elemene for 24 h,significant inhibition of ANG II secretion was observed(P<0.05),but 10 mg/Lβ-elemene had no such effect.β-elemene significantly reduced the amount of AT1R mRNA in HSCs after the treatment for 4,12,and 24 h in a dose-dependent manner.The expression of AT1R protein also decreased after the treatment withβ-elemene for 24 h.β-elemene can inhibit the secretion of ANG II and the gene and protein expression of AT1R,which may be the mechanism by whichβ-elemene prevents the progress of hepaticfibrosis.