Fig. 10: A model depicting the mechanism of cellular response to hemin exposure.

Intracerebral hemolysis results in the release of hemin from ruptured blood cells. Initially, cells respond by activating DNA damage response (DDR) and NF-ĸB pathways, leading to a temporary onset of the senescence like phenotype. This response acts as a critical protective mechanism against the neurotoxic effects of hemin and iron following a brain hemorrhage. This is followed by the stimulation of HO-1, an enzyme responsible for breaking down heme. However, continuous exposure to hemin can cause cells to enter a state of prolonged senescence. Our study demonstrates that a bifunctional carbon nanoparticle comprising anti-oxidant + iron chelating activity (DEF-PEG-OAC) alleviates genome damage and cellular senescence.