Abstract
Following intracerebral hemorrhage, mitigating oxidative stress and removing excess iron are critical strategies for reducing secondary brain injury and improving neurological outcomes. In vitro, we synthesized quercetin-ethylenediamine carbon quantum dots (QECQDs) with diameters of 2-11 nm and found that QECQDs effectively scavenge ABTS+· and DPPH· free radicals, defending HT22 cells against hemin-induced oxidative stress. In vivo, QECQDs predominantly accumulate in the pia mater, subarachnoid space, and dura mater after intrathecal injection. Compared to the ICH injury group, QECQDs treatment effectively improves cerebral blood flow, inhibits oxidative stress damage, and reduces neuron death. Importantly, QECQDs treatment reduced hemorrhage volume, alleviated edema, and improved neurological function. This lays a foundation for developing multi-target drugs for treating ICH.