Open AccessMacrophage‐Disguised Manganese Dioxide Nanoparticles for Neuroprotection by Reducing Oxidative Stress and Modulating Inflammatory Microenvironment in Acute Ischemic Stroke
Author(s) -
Li Chao,
Zhao Zhenhao,
Luo Yifan,
Ning Tingting,
Liu Peixin,
Chen Qinjun,
Chu Yongchao,
Guo Qin,
Zhang Yiwen,
Zhou Wenxi,
Chen Hongyi,
Zhou Zheng,
Wang Yu,
Su Boyu,
You Haoyu,
Zhang Tongyu,
Li Xuwen,
Song Haolin,
Li Chufeng,
Sun Tao,
Jiang Chen
Publication year - 2021
Publication title -
advanced science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.388
H-Index - 100
ISSN - 2198-3844
DOI - 10.1002/advs.202101526
Subject(s) - neuroprotection , penumbra , microglia , oxidative stress , proinflammatory cytokine , reactive oxygen species , macrophage , pharmacology , microbiology and biotechnology , chemistry , medicine , inflammation , materials science , ischemia , immunology , biochemistry , biology , in vitro
Reperfusion injury is still a major challenge that impedes neuronal survival in ischemic stroke. However, the current clinical treatments are remained on single pathological process, which are due to lack of comprehensive neuroprotective effects. Herein, a macrophage‐disguised honeycomb manganese dioxide (MnO 2 ) nanosphere loaded with fingolimod (FTY) is developed to salvage the ischemic penumbra. In particular, the biomimetic nanoparticles can accumulate actively in the damaged brain via macrophage‐membrane protein‐mediated recognition with cell adhesion molecules that are overexpressed on the damaged vascular endothelium. MnO 2 nanosphere can consume excess hydrogen peroxide (H 2 O 2 ) and convert it into desiderated oxygen (O 2 ), and can be decomposed in acidic lysosome for cargo release, so as to reduce oxidative stress and promote the transition of M1 microglia to M2 type, eventually reversing the proinflammatory microenvironment and reinforcing the survival of damaged neuron. This biomimetic nanomedicine raises new strategy for multitargeted combined treatment of ischemic stroke.