AI Article Synopsis
- Oxidative stress significantly impedes recovery from brain damage due to hypoxia-ischemia (HI), but cerium vanadate (CeVO) nanozymes may offer a noninvasive therapeutic solution to this problem, specifically targeting neuronal mitochondria.
- CeVO nanozymes demonstrate protective effects against acute brain injury by inhibiting damaging cellular processes and promoting functional recovery over time, while showing no toxicity to other organs.
- The beneficial effects of CeVO nanozymes are linked to reduced oxidative stress and increased expression of Nrf2, a protein that helps manage oxidative damage; however, blocking Nrf2 negates their protective impact, highlighting its crucial role in therapy.
Article Abstract
Oxidative stress is a major obstacle for neurological functional recovery after hypoxia-ischemia (HI) brain damage. Nanozymes with robust anti-oxidative stress properties offer a therapeutic option for HI injury. However, insufficiency of nanozyme accumulation in the HI brain by noninvasive administration hinders their application. Herein, we reported a cerium vanadate (CeVO) nanozyme to realize a noninvasive therapy for HI brain in neonatal mice by targeting brain neuron mitochondria. CeVO nanozyme with superoxide dismutase activity mainly co-located with neuronal mitochondria 1 h after administration. Pre- and post-HI administrations of CeVO nanozyme were able to attenuate acute brain injury, by inhibiting caspase-3 activation, microglia activation, and proinflammation cytokine production in the lesioned cortex 2 d after HI injury. Moreover, CeVO nanozyme administration led to short- and long-term functional recovery following HI insult without any potential toxicities in peripheral organs of mice even after prolonged delivery for 4 weeks. These beneficial effects of CeVO nanozyme were associated with suppressed oxidative stress and up-regulated nuclear factor erythroid-2-related factor 2 (Nrf2) expression. Finally, we found that Nrf2 inhibition with ML385 abolished the protective effects of CeVO nanozyme on HI injury. Collectively, this strategy may provide an applicative perspective for CeVO nanozyme therapy in HI brain damage via noninvasive delivery.
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| http://dx.doi.org/10.1016/j.jconrel.2023.12.016 | DOI Listing |
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Article Synopsis
- Oxidative stress significantly impedes recovery from brain damage due to hypoxia-ischemia (HI), but cerium vanadate (CeVO) nanozymes may offer a noninvasive therapeutic solution to this problem, specifically targeting neuronal mitochondria.
- CeVO nanozymes demonstrate protective effects against acute brain injury by inhibiting damaging cellular processes and promoting functional recovery over time, while showing no toxicity to other organs.
- The beneficial effects of CeVO nanozymes are linked to reduced oxidative stress and increased expression of Nrf2, a protein that helps manage oxidative damage; however, blocking Nrf2 negates their protective impact, highlighting its crucial role in therapy.
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