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Journal of Nutritional Science and Vitaminology (Tokyo) , 49 , 281286

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Conclusion: Our results indicate a protective effect of IGF-1 against OA pathogenesis by inhibition of NF-B signaling via regulation of the MAPK and PI3K/Akt signaling pathways and prevention of apoptosis by suppression of ROS production

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Reduced Cellular Communication Cells rely on signaling molecules to coordinate repair and renewal

By scavenging harmful ROS and suppressing inflammatory signaling pathways, theaflavins may help mitigate the damage caused by iron overload [44]