Journal
MOLECULES
Volume 28, Issue 16, Pages -Publisher
MDPI
DOI: 10.3390/molecules28166014
Keywords
ferulic acid; apoptosis; autophagy; MAPK pathway
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This study investigated the potential role of ferulic acid (FA) as a means of inducing apoptosis and inhibiting colon cancer induced by CT26 cells. The results showed that FA adjuvant treatment upregulated autophagy-related gene expression, suppressed inflammatory response elements expression, and improved bodyweight, ALT, and AST levels. Furthermore, FA inhibited CT26 cell proliferation and induced apoptosis by activating the phosphorylation of ERK and JNK to enhance BCL-2 and BAX proteins in the apoptosis pathway. These findings suggest that FA could be a promising auxiliary therapeutic agent for colon cancer.
Ferulic acid (FA) is a bioactive compound found in traditional Chinese herbal medicine; for example, it is present in Xinjiang Ferula, but also in strong-flavor Chinese baijiu. FA has been shown to play a crucial role in treating oxidative stress, skin whitening, and eye diseases. In this study, the potential role of FA as a means of inducing apoptosis and inhibiting colon cancer induced by the transplantation of CT26 cells was investigated. The results show that FA adjuvant treatment caused an upregulation in the expression of genes related to autophagy while simultaneously suppressing the expression of inflammatory response elements and improving the bodyweight, glutamic pyruvic transaminase (ALT), and glutamic oxaloacetic transaminase (AST) in vivo. Furthermore, FA inhibited the proliferation of CT26 cells and induced apoptosis, specifically by activating the phosphorylation of ERK and JNK to enhance the essential proteins BCL-2 and BAX in the apoptosis pathway. These results suggest that FA could be a promising auxiliary therapeutic agent for the treatment of colon cancer. Further research is needed to better understand the mechanisms underlying the beneficial effects of FA and its synergistic effects with other compounds.
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