组蛋白H3表达对重金属镉暴露肝癌细胞氧化应激性损伤的影响OA

Objective:To investigate the effect of histone H3 modification on oxidative stress damage in hepatocellular carcino-ma cells Hep3B in a cadmium-exposed microenvironment.Methods:Hep3B were divided into a control group and a 20 ng/mL cadmium chloride(CdCl2)stained group,and cultured for 28 days.Flow cytometry was used to detect oxidative stress(reactive oxygen species,ROS)and apoptosis in each group at the time points of 7,14,21,and 28 day of culture;immunofluorescence was used to determine the expression of histone H3 acetylation in each group at different time points;scratches and CCK-8 were used to determine the activity and proliferative capacity of cells in each group at different time points;and an inhibitor of histone H3 acet-ylation was used to intervene on the stained group at the 7,14,and 21 day for 48 hours.Results:Cadmium exposure led to mor-phological atrophy,increased tentacle and fragmentation of Hep3B cells;cell migration and healing were slowed down;With pro-longed cadmium exposure,ROS and apoptosis levels in the stained group increased significantly compared to those in the con-trol group at the 7,14,and 21 day(P<0.05);there were no significant differences between the ROS and apoptosis levels in the stained group at 28 day and those in the control group(P>0.05);Compared to the control groups,the expression level of protein H3 acetylation in the stained group at the 7 and 14 day significantly increased with the prolongation of the intervention time(P<0.01),and the expression of protein H3 acetylation in the stained group at the 21 and 28 day tended to be in a steady state(P<0.01);and the levels of apoptosis and ROS at the 7,14,and 21 day inhibitor groups were decreased compared to those in the stained group(P<0.01).Conclusion:Low-dose cadmium exposure can induce oxidative stress injury leading to apoptosis in Hep3B hepatocellular carcinoma cells at an early stage,and inhibit the anti-oxidative stress ability of hepatocellular carcinoma cells affecting their cellular activity;in long-term low-dose cadmium exposure,Hep3B hepatocellular carcinoma cells can enhance tolerance and adapt to the hazardous environment to maintain homeostasis through self-regulation;histone H3 acetylation is in-volved in oxidative stress injury and apoptosis of Hep3B hepatocellular carcinoma cells.