Caffeic acid prevents hydrogen peroxide-induced oxidative damage in SH-SY5Y cell line through mitigation of oxidative stress and apoptosis

AIM: The aim of this study was to examine the potential ameliorative effects of caffeic acid (CA) on hydrogen peroxide (H2O2)-induced neurodegeneration in a human SH-SY5Y cell line, as well as possible mechanisms involved. METHOD: Cell proliferation was evaluated by WST-1 assay. The apoptotic index was calculated by TUNEL Assay. Antioxidant parameters were studied by measuring reactive oxygen species (ROS), lipid peroxidation (LPO) levels, and catalase (CAT) activity. The mRNA expression levels of apoptotic and anti-apoptotic genes were studied by qRT-PCR RESULTS: In this study, the pre-treatment with CA significantly suppressed H2O2-stimulated cell death and apoptosis in SH-SY5Y cell line. The mechanism by which CA pretreatment protected the cells from oxidative injury includes the decrease in ROS and LPO levels, increase in CAT activity, down-regulation of mRNA levels of Bax, cytochrome c, cas-3, cas-8, and p53, and up-regulation of anti-apoptotic Bcl-2 gene. CONCLUSION: These results reveal that CA plays a role in the protection from oxidative injury-triggered apoptosis, which makes CA a likely therapeutic compound for treatment or prevention of neurodegenerative disorders associated with oxidative injury (Fig. 5, Ref. 35).

Automated summary

This study demonstrates the protective effects of caffeic acid on hydrogen peroxide-induced neurodegeneration by reducing oxidative stress and increasing antioxidant enzyme activity. Caffeic acid may serve as a potential therapeutic compound for the treatment or prevention of neurodegenerative disorders associated with oxidative injury.