Hepatoprotective effect of p‐Coumaric acid against KBrO3‐induced apoptosis in HepG2 cells

In the present study, we investigated the effect of the p‐Coumaric acid (PCA), a phenolic acid, on potassium bromate (KBrO3) induced oxidative damage, Ras/Raf/MEK signaling, and apoptosis in HepG2 cells. Our findings showed that PCA‐treated cells prevented cytotoxicity compared with KBrO3‐treated ce...

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Published in:Cell biochemistry and function 2023-10, Vol.41 (7), p.868-875
Main Authors: Selvaraj Nivetha, Kumaraswami Radha Thayammal Asha, Srinivasan, Subramani, Raju Murali, Kanagalakshmi, Ambothi
Format: Article
Language:English
Subjects:
Acids
Antioxidants
Apoptosis
Caspase
Coumaric acid
Cytotoxicity
Damage
Deoxyribonucleic acid
DNA
DNA damage
Lipid peroxidation
Lipids
MAP kinase
Oxidative stress
Peroxidation
Phenolic acids
Phenols
Potassium bromate
Raf protein
Toxicity
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Summary:In the present study, we investigated the effect of the p‐Coumaric acid (PCA), a phenolic acid, on potassium bromate (KBrO3) induced oxidative damage, Ras/Raf/MEK signaling, and apoptosis in HepG2 cells. Our findings showed that PCA‐treated cells prevented cytotoxicity compared with KBrO3‐treated cells. Furthermore, KBrO3‐induced oxidative stress and lipid peroxidation was attenuated by PCA and it also increased the antioxidant levels such as SOD, CAT, and GPX. Additionally, PCA inhibited the KBrO3‐induced DNA damage in HepG2 cells. Moreover, PCA treatment suppressed the activation of Ras/Raf/MEK signaling and increased the expression of PRDX‐1. In addition, PCA prevented the KBrO3‐induced apoptosis cascade by altering the expression of proapoptotic, Bax, caspase‐3, and antiapoptotic, Bcl‐2 proteins. The present study proves that PCA inhibited the KBrO3‐induced oxidative stress, DNA damage, and apoptotic signaling cascade in HepG2 cells.
ISSN:0263-6484
1099-0844
DOI:10.1002/cbf.3837