An Intrinsic Therapy of Gold Nanoparticles in Focal Cerebral Ischemia-Reperfusion Injury in Rats

被引:44
作者
Liu, Zhengxia [1 ]
Shen, Yujie [1 ]
Wu, Yucheng [1 ]
Yang, Yujiao [1 ]
Wu, Jin [1 ]
Zhou, Ping [1 ]
Lu, Xiang [1 ]
Guo, Zhirui [1 ]
机构
[1] Nanjing Med Univ, Affiliated Hosp 2, Dept Geriatr, Nanjing 210029, Jiangsu, Peoples R China
基金
美国国家科学基金会;
关键词
Ischemia-Reperfusion Injury; Stroke; Gold Nanoparticles; Inflammation; Apoptosis; DNA FRAGMENTATION; MAGNETIC NANOPARTICLES; GLOBAL-ISCHEMIA; SIZE; CYTOTOXICITY; MITOCHONDRIA; TOXICITY; BIOLOGY; STRESS; STROKE;
D O I
10.1166/jbn.2013.1597
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Ischemic stroke is a leading cause of death and disability, and the treatment options are limited. Recent studies demonstrated that the promising applications of gold nanoparticles (Au-NPs) as intrinsic therapeutics; however, little is known about the effect of Au-NPs on cerebral ischemia-reperfusion (I/R) injury. In this paper, the role of Au-NPs on cerebral I/R injury in the rat middle cerebral artery occlusion (MCAO) model was investigated using citrate-capped 5 nm and 20 nm Au-NPs. It was found that 20 nm Au-NPs administration led to remarkable amelioration of neurologic deficits and infarction volumes. Further research revealed that 20 nm Au-NPs elevated the production of anti-inflammatory cytokines, as well as inhibited I/R induced activation of astrocytes and microglias. Moreover, the expressions of anti-apoptotic proteins were up-regulated and the pro-apoptotic molecules were down-regulated in the post-ischemic brains. These effects were opposite in 5 nm group. The above results showed that the neuroprotection of 20 nm Au-NPs was attributable to its anti-inflammatory and anti-apoptotic effect. This study could provide a novel strategy for the treatment of cerebral I/R injury.
引用
收藏
页码:1017 / 1028
页数:12
相关论文
共 48 条
[1]   Functional diversity of helper T lymphocytes [J].
Abbas, AK ;
Murphy, KM ;
Sher, A .
NATURE, 1996, 383 (6603) :787-793
[2]   Toxicity and cellular uptake of gold nanoparticles: what we have learned so far? [J].
Alkilany, Alaaldin M. ;
Murphy, Catherine J. .
JOURNAL OF NANOPARTICLE RESEARCH, 2010, 12 (07) :2313-2333
[3]   Intrinsic therapeutic applications of noble metal nanoparticles: past, present and future [J].
Arvizo, Rochelle R. ;
Bhattacharyya, Sanjib ;
Kudgus, Rachel A. ;
Giri, Karuna ;
Bhattacharya, Resham ;
Mukherjee, Priyabrata .
CHEMICAL SOCIETY REVIEWS, 2012, 41 (07) :2943-2970
[4]   JNK inhibition and inflammation after cerebral ischemia [J].
Benakis, Corinne ;
Bonny, Christophe ;
Hirt, Lorenz .
BRAIN BEHAVIOR AND IMMUNITY, 2010, 24 (05) :800-811
[5]   Stroke prevention: an update [J].
Marie-Germaine Bousser .
Frontiers of Medicine, 2012, 6 (1) :22-34
[6]   In vivo induction of heat shock proteins in the substantia nigra following L-DOPA administration is associated with increased activity of mitochondrial complex I and nitrosative stress in rats:: regulation by glutathione redox state [J].
Calabrese, Vittorio ;
Mancuso, Cesare ;
Ravagna, Agrippino ;
Perluigi, Marzia ;
Cini, Chiara ;
De Marco, Carlo ;
Butterfield, Allan ;
Stella, Anna Maria Giuffrida .
JOURNAL OF NEUROCHEMISTRY, 2007, 101 (03) :709-717
[7]   Heat shock protein 60 or 70 activates nitric-oxide synthase (NOS) I- and inhibits NOSII-associated signaling and depresses the mitochondrial apoptotic cascade during brain stem death [J].
Chan, Julie Y. H. ;
Cheng, Hsiao-Lei ;
Chou, Jimmy L. J. ;
Li, Faith C. H. ;
Dai, Kuang-Yu ;
Chan, Samuel H. H. ;
Chang, Alice Y. W. .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2007, 282 (07) :4585-4600
[8]   Mitochondria and neuronal death/survival signaling pathways in cerebral ischemia [J].
Chan, PH .
NEUROCHEMICAL RESEARCH, 2004, 29 (11) :1943-1949
[9]   Regulated portals of entry into the cell [J].
Conner, SD ;
Schmid, SL .
NATURE, 2003, 422 (6927) :37-44
[10]   Treatment of stroke with a PSD-95 inhibitor in the gyrencephalic primate brain [J].
Cook, Douglas J. ;
Teves, Lucy ;
Tymianski, Michael .
NATURE, 2012, 483 (7388) :213-U112