Fungal Toxins And Athero-sclerosis Incidence Relations Research Progress

ObjectiveThe objective of the current study was to investigate the direct effects ofCIT on apoptosis of vascular endothelial cells in vitro and to explore theunderlying mechanisms.Methods1.HUVECs were cultured in DMEM medium， and treated by citreoviridin(CIT)2.The growth inhibitory effect of CIT on HUVECs was assessed by MTT.3.Cell cycle and cell apoptosis were detected by flow cytometry (FCM).4.Western blotting analysis was carried out to analyze Bax、 Bcl-2、Caspase-3、Caspase-7、Caspase-9，PARP.Result1.CIT inhibited the growth of HUVECs in a dose-and time-dependentmanner (P<0.05). CIT treatment resulted in the accumulation of HUVECs in theG0/G1phase， and cell numbers in S-phase were decreased significantly(P<0.05).2.CIT can cause apoptosis of HUVECs in different doses or time. Theeffect of apoptosis was more obvious in higher level CIT (P<0.05).3.Treatment of HUVECs with CIT resulted in decreasing levels ofanti-apoptotic Bcl-2protein(P<0.05). The expression of the pro-apoptotic Baxprotein was up-regulated significantly after CIT treatment(P<0.05).4.The cleavage of apical pro-caspase-9and-3into the characteristicactivate fragments was already evident after treatment with CIT. The cleavage of PARP is increased by CIT.Conclusion1.CIT induces the accumulation of HUVECs in the G0/G1phase, andblocks cell division cycle. The dose-dependent effect results in the decreasedcell proliferation.2.These results suggest that CIT can damage HUVECs by inducingapoptosis of the cells.CIT induce apoptosis of HUVECs in a dose-dependentmanner.3.The signal pathway of CIT treated apoptosis: the modulatory effect ofCIT one HUVECs apoptosis is through Bax and Bcl-2，and result in significantactivation of caspase-9and caspase--3, which induce cleavage of PARP.