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image of Prooxidant Activity of Gallic Acid by Promote Reactive Oxygen Species, Apoptosis and Autophagy in HepG2 Cells In Vitro

Abstract

IntroductionGallic acid (GA), a natural phenolic acid, has been reported as an antitumor in various cancer cells. Although some mechanism such as apoptosis is well known but detail of other mechanism such as their pro-oxidant and autophagy activity are still considerable.

Methods

pro-oxidative activity and the anti-proliferative activity in GA on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (II) and Fe (II) were measured. Furthermore, colony forming, ROS generation, apoptosis induction, autophagy and mitochondrial membrane potential (MMP) were examined.

Results

HepG2 cells treated with GA + Cu (II) reduced the cells viability significantly ( <0.001). GA +Cu (II) could induce HepG2 cell morphological changes, and stimulate apoptotic cell death. Moreover, GA +Cu (II) triggered the mitochondrial-dependent apoptotic pathway, by increasing the level of intracellular ROS and disruption of MMP. Furthermore, GA+ Cu (II) reduced the Plating Efficiency and Surviving Fraction significantly and also increases autophagic vacuoles in the HepG2 cells.

Conclusion

According to our results, GA played pro-oxidant role in presence of Cu (II), also it could trigger apoptosis by increased ROS and disruption of MMP. This combination also induced autophagy in HepG2. These effects might be a promising in future of anticancer research.

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2024-10-30
2024-11-26
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  • Article Type:
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Keywords: pro-oxidant ; reactive oxygen specious ; copper ; autophagy ; apoptosis ; Gallic acid
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