Would Colloidal Gold Nanocarriers Present An Effective Diagnosis Or Treatment For Ischemic Stroke?

被引:142
作者
Amani, Hamed [1 ,2 ]
Mostafavi, Ebrahim [3 ]
Alebouyeh, Mahmoud Reza [4 ]
Arzaghi, Hamidreza [5 ]
Akbarzadeh, Abolfazl [6 ]
Pazoki-Toroudi, Hamidreza [2 ,7 ]
Webster, Thomas J. [3 ]
机构
[1] Iran Univ Med Sci, Fac Adv Technol Med, Dept Med Nanotechnol, Tehran, Iran
[2] Iran Univ Med Sci, Fac Med, Physiol Res Ctr, Tehran, Iran
[3] Northeastern Univ, Dept Chem Engn, Boston, MA 02115 USA
[4] Iran Univ Med Sci, Fac Med, Anesthesia Dept, Tehran, Iran
[5] Iran Univ Med Sci, Fac Allied Med Sci, Dept Med Biotechnol, Tehran, Iran
[6] Tabriz Univ Med Sci, Fac Adv Med Sci, Dept Med Nanotechnol, Tabriz, Iran
[7] Iran Univ Med Sci, Fac Med, Dept Physiol, Tehran, Iran
关键词
targeted delivery; gold nanoparticles; necroptosis; surface charge; oxidative stress; cytotoxicity; BLOOD-BRAIN-BARRIER; OXIDATIVE STRESS; REPERFUSION INJURY; HIPPOCAMPAL ISCHEMIA; PARTICLE-SIZE; STEM-CELLS; NANOPARTICLES; CYTOTOXICITY; NECROPTOSIS; SURFACE;
D O I
10.2147/IJN.S210035
中图分类号
TB3 [工程材料学];
学科分类号
082905 [生物质能源与材料];
摘要
Introduction: This study was conducted to evaluate OX26-PEG-coated gold nanoparticles (GNPs) (OX26@GNPs) as a novel targeted nanoparticulate system on cell survival after ischemic stroke. Materials and methods: Dynamic light scattering (DLS), zeta sizer, and transmission electron microscopy (TEM) were performed to characterize the OX26@GNPs. The effect of OX26@GNPs on infarct volume, neuronal loss, and necroptosis was evaluated 24 h after reperfusion using 2, 3,5-Triphenyltetrazolium chloride (TTC) staining, Nissl staining and Western blot assay, respectively. Results: Conjugation of OX26-PEG to the surface of the 25 nm colloidal gold particles increased their size to 32 +/- 2 nm, while a zeta potential change of -40.4 to 3.40 mV remarkably increased the stability of the nanoparticles. Most importantly, OX26@GNPs significantly increased the infarcted brain tissue, while bare GNPs and PEGylated GNPs had no effect on the infarct volume. However, our results indicated an extension of necroptotic cell death, followed by cell membrane damage. Conclusion: Collectively, our results showed that the presently formulated OX26@GNPs are not suitable nanocarriers nor contrast agents under oxidative stress for the diagnosis and treatment of ischemic stroke. Moreover, our findings suggest that the cytotoxicity of GNPs in the brain is significantly associated with their surface charge.
引用
收藏
页码:8013 / 8031
页数:19
相关论文
共 64 条
[61]
CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis [J].
Zhang, Ting ;
Zhang, Yan ;
Cui, Mingyao ;
Jin, Li ;
Wang, Yimei ;
Lv, Fengxiang ;
Liu, Yuli ;
Zheng, Wen ;
Shang, Haibao ;
Zhang, Jun ;
Zhang, Mao ;
Wu, Hongkun ;
Guo, Jiaojiao ;
Zhang, Xiuqin ;
Hu, Xinli ;
Cao, Chun-Mei ;
Xiao, Rui-Ping .
NATURE MEDICINE, 2016, 22 (02) :175-182
[62]
RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome [J].
Zhang, Yingying ;
Su, Sheng Sean ;
Zhao, Shubo ;
Yang, Zhentao ;
Zhong, Chuan-Qi ;
Chen, Xin ;
Cai, Qixu ;
Yang, Zhang-Hua ;
Huang, Deli ;
Wu, Rui ;
Han, Jiahuai .
NATURE COMMUNICATIONS, 2017, 8
[63]
Melatonin protects cardiac microvasculature against ischemia/reperfusion injury via suppression of mitochondrial fission-VDAC1-HK2-mPTP-mitophagy axis [J].
Zhou, Hao ;
Zhang, Ying ;
Hu, Shunying ;
Shi, Chen ;
Zhu, Pingjun ;
Ma, Qiang ;
Jin, Qinhua ;
Cao, Feng ;
Tian, Feng ;
Chen, Yundai .
JOURNAL OF PINEAL RESEARCH, 2017, 63 (01)
[64]
Ripk3 promotes ER stress-induced necroptosis in cardiac IR injury: A mechanism involving calcium overload/XO/ROS/mPTP pathway [J].
Zhu, Pingjun ;
Hu, Shunying ;
Jin, Qinhua ;
Li, Dandan ;
Tian, Feng ;
Toan, Sam ;
Li, Yang ;
Zhou, Hao ;
Chen, Yundai .
REDOX BIOLOGY, 2018, 16 :157-168