Fig. 3

Apigenin holds promise in the treatment of ischemic stroke by modulating RAD51 and BRCA1 during HRR as well as Ku70/80 in NHEJ. It activates the p53 pathway, which may elevate the transcriptional activity of BRCA1, thereby indirectly regulating the expression of RAD51 and enhancing DNA repair processes. Additionally, apigenin upregulates the expression of Ku70/80 via the p53 pathway, further promoting DNA repair. It potentially inhibits cancer cell proliferation by suppressing the PI3K/Akt signaling pathway and decreasing cellular reliance on growth signals, thereby modulating the expression of BRCA1 and RAD51. Additionally, it exhibits anti-inflammatory properties, likely through the inhibition of NF-κB activity and the reduction of DNA damage induced by inflammation, thus safeguarding the functions of BRCA1, RAD51, and Ku70/80 and enhancing DNA repair mechanisms. It may modulate the expression and repair functions of BRCA1, RAD51, and Ku70/80 through the regulation of the ERK/MAPK signaling pathway. Additionally, it activates the AMPK pathway, thereby enhancing the expression of Ku70/80 and associated proteins, which contributes to increased DNA repair. Furthermore, it indirectly facilitates Ku70 expression by eliminating oxygen free radicals and mitigating oxidative DNA damage