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To investigate the molecular mechanism of endosulfan damaging endothelial cell, human umbilical vein endothelial cells (HUVECs) were exposed to 1,6, 12 μg/mL endosulfan, 12 μg/mL endosulfan + γ-secretase inhibitor (DAPT) (20μM)and 12 μg/mL endosulfan + N-Acetyl-L-cysteine (NAC) (3mM) for 24 h, respectively.The results showed that endosulfan increased the LDH release and reactive oxygen species (ROS) production, led to the increases of malondialdehyde (MDA) level and apoptosis rate, while NAC could attenuate the above changes.Endosulfan resulted in the arrest of both S and G2/M phases, induced the proliferation inhibition and blocked the mitosis process, but DAPT relieved the G2/M phase arrest and proliferation inhibition caused by endosulfan.The protein expressions of Jagged1, Dl14, Notch1,Cleaved-Notchl, Notch4, Hes1 and p21 in HUVECs increased remarkably after endosulfan treatment, while decreased by the presence of DAPT or NAC, respectively.The results suggested that endosulfan could induce cell cycle arrest and proliferation inhibition via the Notch signaling pathway resulting from oxidative stress, which could be one of the mechanisms behind cardiovascular toxicity induced by endosulfan.