This paper focused on the biodistribution of the cross-linked hyaluronic acid (HA-NPs) sub-micron particles in tumor-bearing mice. Solvent-non solvent method followed glutaraldehyde cross-linking utilized for the fabrication of HA-NPs. Size measurement and morphological analysis were performed by dynamic light scattering and electron microscopy, respectively and the size found to be in the range of 200-400 nm. In vitro viability in LNCaP cell line was assessed by water soluble tetrazolium assay after 24 h of exposure to sub-micron particles and no toxicity was found to higher concentration of 3 mg/mL. Internalization of particles in prostate cancer cell LNCaP were studied by confocal microscopy with FITC labeled submicron particles and involvement of hyaluronan receptor mediated uptake/endocytosis was confirmed by competitive assay. Biodistribution studies were performed in xenograft prostate cancer mice model with fluorophore labeled particles and monitored in tumoral parenchyma with strong fluorescence, meanwhile very less signal in liver, kidney and spleen while no fluorescence found in lung after 24 h of systemic administration; that shown ability of this HA based system to recognize cancer tissue. These result fetched that hyaluronic acid based system is selective for tumoral site and can be utilized to deliver bioactives in specific (targeting) and controlled (temporal) manner to cancerous tissue.
We evaluated the effects of treatment with the inner ester derivative of the monosialoganglioside GM1 on cortical electroencephalographic activity and hippocampal CA1 morphology after transitory, near-complete cerebral ischemia in rats. Ischemia was induced by the four-vessel occlusion method, and we studied only the 58 rats that showed amino acid neurotransmission plays an important role. Neurons selectively vulnerable to an ischemic episode receive prominent excitatory amino acid transmitter inputs, and ablation of these pathways reduces ischemia-induced neuronal loss. In addition, the extracellular concentrations of glutamate and aspartate -potential neurotoxins both in vitro and in vivo -increase during ischemia. A current hypothesis is that excessive accumulation of glutamate or related compounds, via specific postsynaptic receptors, cause neuronal overactivation, triggering a cascade of cellular events that ultimately lead to cell death. 1 A corollary to the above hypothesis is that agents capable of antagonizing specific excitatory amino acid receptor-related recognition sites or postreceptor effects may be of potential therapeutic value. In particular, great attention has recently been focused on Af-methyl-D-aspartate (NMDA) receptor antago-
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.