Carbon dot targeting to nitrogen signaling molecules for inhibiting neuronal death

Free radical-induced oxidative damage and nitrosative stress have been identified as key factors in neuroinflammation responses after traumatic brain injury (TBI), with which reactive oxygen and nitrogen species (RONS), especially nitrogen signaling molecules, are strongly associated. Here, we prepa...

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Veröffentlicht in:Journal of materials chemistry. B, Materials for biology and medicine Materials for biology and medicine, 2020-03, Vol.8 (11), p.2321-233
Hauptverfasser: Ouyang, Lufei, Mu, Xiaoyu, Wang, Junying, Li, Qifeng, Gao, Yalong, Liu, Haile, Sun, Si, Ren, Qinjuan, Yan, Ruijuan, Wang, Jingya, Liu, Qiang, Sun, Yuanming, Liu, Changlong, He, Hua, Long, Wei, Zhang, Xiao-Dong
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container_issue 11
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container_title Journal of materials chemistry. B, Materials for biology and medicine
container_volume 8
creator Ouyang, Lufei
Mu, Xiaoyu
Wang, Junying
Li, Qifeng
Gao, Yalong
Liu, Haile
Sun, Si
Ren, Qinjuan
Yan, Ruijuan
Wang, Jingya
Liu, Qiang
Sun, Yuanming
Liu, Changlong
He, Hua
Long, Wei
Zhang, Xiao-Dong
description Free radical-induced oxidative damage and nitrosative stress have been identified as key factors in neuroinflammation responses after traumatic brain injury (TBI), with which reactive oxygen and nitrogen species (RONS), especially nitrogen signaling molecules, are strongly associated. Here, we prepared ultrasmall carbon dot (CD) by using a simple and facile method. In vitro assessment experiments show that the antioxidative CD exhibits an ultrahigh target-scavenging effect for nitrogen signaling molecules, especially the highly reactive &z.rad;NO and ONOO − . However, CD can only partially eliminate conventional oxygen radials such as O 2 &z.rad; − and &z.rad;OH, indicating CD has a preference for RNS modulation. Moreover, in vitro cell experiments and in vivo mice experiments reveal that CD can reduce the reactive oxygen species (ROS) level and lipid peroxidation, enhance superoxide dismutase (SOD) activity and GSSG level, and further improve the survival rate of neuron cells and TBI mice. These results declare that antioxidative CD could serve as an effective therapeutic for TBI. Ultrasmall carbon dot with targeting ability to nitrogen signaling molecules inhibit neuronal death by regulating the activity of endogenous enzymes.
doi_str_mv 10.1039/c9tb02447f
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Here, we prepared ultrasmall carbon dot (CD) by using a simple and facile method. In vitro assessment experiments show that the antioxidative CD exhibits an ultrahigh target-scavenging effect for nitrogen signaling molecules, especially the highly reactive &amp;z.rad;NO and ONOO − . However, CD can only partially eliminate conventional oxygen radials such as O 2 &amp;z.rad; − and &amp;z.rad;OH, indicating CD has a preference for RNS modulation. Moreover, in vitro cell experiments and in vivo mice experiments reveal that CD can reduce the reactive oxygen species (ROS) level and lipid peroxidation, enhance superoxide dismutase (SOD) activity and GSSG level, and further improve the survival rate of neuron cells and TBI mice. These results declare that antioxidative CD could serve as an effective therapeutic for TBI. 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B, Materials for biology and medicine</title><addtitle>J Mater Chem B</addtitle><description>Free radical-induced oxidative damage and nitrosative stress have been identified as key factors in neuroinflammation responses after traumatic brain injury (TBI), with which reactive oxygen and nitrogen species (RONS), especially nitrogen signaling molecules, are strongly associated. Here, we prepared ultrasmall carbon dot (CD) by using a simple and facile method. In vitro assessment experiments show that the antioxidative CD exhibits an ultrahigh target-scavenging effect for nitrogen signaling molecules, especially the highly reactive &amp;z.rad;NO and ONOO − . However, CD can only partially eliminate conventional oxygen radials such as O 2 &amp;z.rad; − and &amp;z.rad;OH, indicating CD has a preference for RNS modulation. Moreover, in vitro cell experiments and in vivo mice experiments reveal that CD can reduce the reactive oxygen species (ROS) level and lipid peroxidation, enhance superoxide dismutase (SOD) activity and GSSG level, and further improve the survival rate of neuron cells and TBI mice. These results declare that antioxidative CD could serve as an effective therapeutic for TBI. 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However, CD can only partially eliminate conventional oxygen radials such as O 2 &amp;z.rad; − and &amp;z.rad;OH, indicating CD has a preference for RNS modulation. Moreover, in vitro cell experiments and in vivo mice experiments reveal that CD can reduce the reactive oxygen species (ROS) level and lipid peroxidation, enhance superoxide dismutase (SOD) activity and GSSG level, and further improve the survival rate of neuron cells and TBI mice. These results declare that antioxidative CD could serve as an effective therapeutic for TBI. Ultrasmall carbon dot with targeting ability to nitrogen signaling molecules inhibit neuronal death by regulating the activity of endogenous enzymes.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>32100792</pmid><doi>10.1039/c9tb02447f</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-7212-0138</orcidid></addata></record>
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source MEDLINE; Royal Society Of Chemistry Journals 2008-
subjects Animals
Antioxidants - chemistry
Antioxidants - pharmacology
Biological Transport
Blood-Brain Barrier - metabolism
Brain Injuries, Traumatic - drug therapy
Carbon - chemistry
Carbon dots
Cell Death - drug effects
Cysteine - chemistry
Disease Models, Animal
Experiments
Free radicals
Free Radicals - chemistry
Free Radicals - metabolism
Head injuries
Humans
In vitro methods and tests
Inflammation
Lipid peroxidation
Lipid Peroxidation - drug effects
Lipids
Lysine - chemistry
Mice
Mice, Inbred C57BL
Morris Water Maze Test - drug effects
Neurons - cytology
Nitrogen
Oxidative Stress - drug effects
Oxygen
Peroxidation
Quantum Dots - chemistry
Quantum Dots - metabolism
Reactive nitrogen species
Reactive Nitrogen Species - chemistry
Reactive Nitrogen Species - metabolism
Reactive oxygen species
Reactive Oxygen Species - chemistry
Reactive Oxygen Species - metabolism
Scavenging
Signaling
Superoxide dismutase
Superoxide Dismutase - metabolism
Tissue Distribution
Traumatic brain injury
title Carbon dot targeting to nitrogen signaling molecules for inhibiting neuronal death
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