Ceria Nanoparticles that can Protect against Ischemic Stroke

Kim, Chi Kyung; Kim, Sang Woo; Choi, In‐Young; Soh, Min; Kim, Dohoung; Kim, Young‐Ju; Jang, Hyunduk; Yang, H M; Kim, Jun Yup; Park, Hong‐Kyun; Park, Seung Pyo; Park, Sangseung; Yu, Taekyung; Yoon, Byung‐Woo; Lee, Seung‐Hoon; Hyeon, Taeghwan

doi:10.1002/ange.201203780

Cited by 67 publications

(68 citation statements)

References 31 publications

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“…An increase in the population of Annexin V þ and PI þ cells was observed at higher dose of QCA. It is well known that ROS production and apoptosis are closely related and activation of caspase-3 is one of hallmark consequences of GSH depletion 35,36 . Therefore, the superior apoptosis-inducing potential of QCA is attributed to the combined effects of GSH-depleting QM and ROS-generating cinnamaldehyde.…”

Section: Resultsmentioning

confidence: 99%

Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death

et al. 2015

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Cancer cells, compared with normal cells, are under oxidative stress associated with the increased generation of reactive oxygen species (ROS) including H 2 O 2 and are also susceptible to further ROS insults. Cancer cells adapt to oxidative stress by upregulating antioxidant systems such as glutathione to counteract the damaging effects of ROS. Therefore, the elevation of oxidative stress preferentially in cancer cells by depleting glutathione or generating ROS is a logical therapeutic strategy for the development of anticancer drugs. Here we report a dual stimuli-responsive hybrid anticancer drug QCA, which can be activated by H 2 O 2 and acidic pH to release glutathione-scavenging quinone methide and ROS-generating cinnamaldehyde, respectively, in cancer cells. Quinone methide and cinnamaldehyde act in a synergistic manner to amplify oxidative stress, leading to preferential killing of cancer cells in vitro and in vivo. We therefore anticipate that QCA has promising potential as an anticancer therapeutic agent.

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Section: Resultsmentioning

confidence: 99%

Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death

et al. 2015

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“…Values listed under blots represent relative ratios of p-DRP1 S616 to total DRP1 protein normalized to actin nanoparticles to cross the BBB strikingly increased after injury (resulting in increased ROS/RNS). 57,58 By contrast, another study reported very small (2.9 nm diameter), citrate/ EDTA-stabilized CeO 2 nanoparticles administered intravenously to healthy rats appeared to cross the intact BBB, 56 suggesting that particle modifications might help improve neuronal delivery. In sum, considering the variability in findings to date, efficient delivery of nanoceria to neurons remains an important issue requiring further research and investigation.…”

Section: Discussionmentioning

confidence: 98%

“…[56][57][58] In two of these studies, CeO 2 nanoparticles were administered intravenously and the concentration of nanoparticles was very low in the normal brain. 57,58 The study by Kim et al 57 used nanoceria that were surface modified with an artificial polymer phospholipid-polyethylene glycol, which is often added to nanoparticles to improve uptake and biodistribution, 59 yet these particles were also found only in low amounts in brain tissue. However, the ability of (a) Western blots of p-DRP1 S616, total DRP1 and actin protein levels from neurons exposed for 3 h to aged SNOC (100 mM), nanoceria (100 nM; 3 h pretreatment) or fresh SNOC (100 mM) alone or a combination of nanoceria (100 nM) and fresh SNOC (100 mM).…”

Section: Discussionmentioning

confidence: 99%

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

et al. 2014

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Evidence indicates that nitrosative stress and mitochondrial dysfunction participate in the pathogenesis of Alzheimer's disease (AD). Amyloid beta (Ab) and peroxynitrite induce mitochondrial fragmentation and neuronal cell death by abnormal activation of dynamin-related protein 1 (DRP1), a large GTPase that regulates mitochondrial fission. The exact mechanisms of mitochondrial fragmentation and DRP1 overactivation in AD remain unknown; however, DRP1 serine 616 (S616) phosphorylation is likely involved. Although it is clear that nitrosative stress caused by peroxynitrite has a role in AD, effective antioxidant therapies are lacking. Cerium oxide nanoparticles, or nanoceria, switch between their Ce 3 þ and Ce 4 þ states and are able to scavenge superoxide anions, hydrogen peroxide and peroxynitrite. Therefore, nanoceria might protect against neurodegeneration. Here we report that nanoceria are internalized by neurons and accumulate at the mitochondrial outer membrane and plasma membrane. Furthermore, nanoceria reduce levels of reactive nitrogen species and protein tyrosine nitration in neurons exposed to peroxynitrite. Importantly, nanoceria reduce endogenous peroxynitrite and Ab-induced mitochondrial fragmentation, DRP1 S616 hyperphosphorylation and neuronal cell death.

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“…Kim et al 91 reported that CeONP can protect against ischemic stroke. Cerebral ischemia, or stroke, caused by a reduction of blood flow to the brain because of a clot or hemorrhage is the third leading cause of death worldwide.…”

Section: Cerium Oxide Nanoparticle C Xu and X Qumentioning

confidence: 99%

Cerium oxide nanoparticle: a remarkably versatile rare earth nanomaterial for biological applications

2014

NPG Asia Mater

927

650

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Ceria Nanoparticles that can Protect against Ischemic Stroke

Cited by 67 publications

References 31 publications

Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death

Amplification of oxidative stress by a dual stimuli-responsive hybrid drug enhances cancer cell death

Cerium oxide nanoparticles protect against Aβ-induced mitochondrial fragmentation and neuronal cell death

Cerium oxide nanoparticle: a remarkably versatile rare earth nanomaterial for biological applications

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