<p>Would Colloidal Gold Nanocarriers Present An Effective Diagnosis Or Treatment For Ischemic Stroke?</p>

Abstract

IntroductionThis 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 methodsDynamic 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.ResultsConjugation 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.ConclusionCollectively, 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.

<p>TiO₂ Nanotubes Alleviate Diabetes-Induced Osteogenetic Inhibition</p>

“…36 Amani et al showed that surface charge played an important role in cell survival. 37 Li et al reported enhanced bioactivity on the TiO 2 surface with more negative zeta potential. 38 Referring to the zeta potential of the different modified Ti surfaces reported in the above articles in conjunction with the results of the present study, we found that the lower the zeta potential of the surface, the stronger the osseointegration ability.…”

Investigating the Relationship Between Neuronal Cell Death and Early DNA Methylation After Ischemic Injury

“…Thrombolytic therapy using tissue plasminogen activator (t-PA) is known as a promising treatment for ischemic stroke. However, t-PA has narrow therapeutic time window because of its severe hemorrhagic side effects that induce inflammation of brain capillaries and subsequently severe injury to neurons after stroke (Amani et al, 2019b). Therefore, the use of t-PA is restricted to selected patients only, and patients who have not been treated with t-PA will suffer from serious aftereffects.…”

Protective Effects of Yiqi Xingnao Oral Liquid on Cerebral Ischemia‐Reperfusion Injury in Rats and Its Related Mechanisms

“…Furthermore, the blood-brain barrier, consisting of endothelial cells, tight junctions, astrocytic end-feet processes, pericytes, and basement membrane, is essential in regulation of the passage of inflammatory cytokines, proteins, and ions between the brain and plasma [23]. Studies have shown that disruption of the blood-brain barrier in ischemic stroke could increase the permeability and change the microenvironment of the brain, which may contribute to the further development of brain damage [5][6][7][8][9][10][11][12]24]. Zhang et al demonstrated that a novel IL-1RA-PEP fusion protein could effectively improve cerebral I/R injury by inhibiting the blood-brain barrier permeability [25].…”