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ROS-Dependent Cell Death Induced by Parthenolide in Human Hepatoma Cell HepG2

DOI: 10.4236/oalib.1106025, PP. 1-18

Subject Areas: Molecular Biology

Keywords: Parthenolide, ROS, Cell Death

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With the increase of the action time and dosing concentration, the proliferation of HepG2 cell was inhibited and its vitality gradually decreased. FCM showed that, with the increase of PN action time, the MMP gradually decreased; calcium ions flowed inwards; the cell cycle was arrested in phase G1; the cell apoptosis rate, especially late apoptosis and necrotic cells, increased. The shear expression of apoptosis-related proteins caspase3 and caspase9 was up-regulated; the shear expression of AIF, MIF and PARP1 proteins associated with Caspase-independent apoptosis, i.e. Parthanatos apoptosis, showed time-dependent up-regulation; the long and short expressions of anti-apoptosis protein FLIP showed different degrees of decrease; the ex-pression of autophagy-related proteins LC3A/B and becin-1 was up-regulated; the expression of P62 protein was down-regulated; the expression of cycle- related proteins P53, P27 and P21 increased significantly; the expression of CyclinD1 and CyclinE1 decreased. FCM was used to detect the increase of ROS with the action time of PN; and its generation level showed an increasing trend; after the combination with ROS scavenger NAC, there was no significant difference in cell viability with the control group. There was no significant difference in the expression level of relevant cell death protein with DMSO control group. There was no difference in intracellular ROS generation level with the control group. Conclusion: PN induces the ROS generation in HepG2 cell, blocks its cycle and causes apoptosis and au-tophagy to play an anti-tumor effect.

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Xu, W. , Ge, K. , Guo, Y. , Zhu, W. , Liu, L. and Zhou, Y. (2020). ROS-Dependent Cell Death Induced by Parthenolide in Human Hepatoma Cell HepG2. Open Access Library Journal, 7, e6025. doi:


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