Observing Malondialdehyde-Mediated Signaling Pathway in Cerebral Ischemia Reperfusion Injury with a Specific Nanolight

Abstract

Cerebral ischemia reperfusion injury (CIRI) is closely related to lipid peroxidation. Malondialdehyde (MDA), as a biomarker of lipid peroxidation, is prone to addition with biomacromolecules, resulting in a secondary cerebral injury. However, desirable tools for in vivo-determining cerebral MDA are scarce. Thus, we devised innovative polymer carbon dots carbonized by benzoyl hydrazine and named them BH-PCDs. BH-PCDs covered with hydrazine groups directly form from one-pot synthesis. The functional nanoparticle specifically identifies MDA via a photoinduced electron transfer (PET) mechanism from other similar biological species, especially reactive carbonyl species. BH-PCDs afforded several valuable traits of a simple preparation, a large two-photon absorption cross section, and exceptional biocompatibility, as well as the ability of traversing the blood-brain barrier. Relying on BH-PCDs, we real-time portrayed the increased cerebral MDA under CIRI. Furthermore, combining with a commercial indicator of the superoxide anion (O2•-), an O2•--regulated MDA level under CIRI was visualized in vivo. Moreover, we demonstrated MDA inactivated glutamine synthetase under CIRI, mediating the glutamate level. Overall, we provide a perspective nanolight serviceable for treating CIRI, which could reveal the physiopathology mechanism of brain MDA.