ABSTRACT
Nanotechnology is currently a field of endeavour that has reached a maturation phase beyond the initial hypotheses with an undercurrent challenge to optimise the safety, and scalability for production and clinical trials. Lipid-based nanoparticles (LNP), namely solid lipid nanoparticles (SLN) and nanostructured lipid (NLC), carriers are presently among the most attractive and fast-growing areas of research. SLN and NLC are safe, biocompatible nanotechnology-enabled platforms with ubiquitous applications. This review presents a modern vision that starts with a brief description of characteristics, preparation strategies, and composition ingredients, benefits, and limitations. Next, a discussion of applications and functionalization approaches for the delivery of therapeutics via different routes of delivery. Additionally, the review presents a concise perspective into limitations and future advances. A brief recap on the prospects of molecular dynamics simulations in better understanding NP bio-interface interactions is provided. Finally, the alliance between 3D printing and nanomaterials is presented here as well.
Subject(s)
Nanoparticles , Nanostructures , Drug Carriers , Lipids , LiposomesABSTRACT
Multiple sclerosis is a chronic inflammatory neurodegenerative disease of the central nervous system which injures the myelin sheath. Telmisartan and nifedipine are antihypertensive drugs that recently showed neuroprotective properties against neurodegenerative diseases. This study evaluated the neuroprotective effect of telmisartan or nifedipine in cuprizone-induced demyelination in mice by examining the underlying mechanisms. C57BL/6 mice received a diet containing 0.7% (w/w) cuprizone for 7 days followed by 3 weeks on a 0.2% cuprizone diet. Telmisartan (5 mg/kg/day, p.o.) or nifedipine (5 mg/kg/day, p.o.) was administered for 3 weeks starting from the second week. Telmisartan or nifedipine improved locomotor activity and enhanced motor coordination as demonstrated by open field, rotarod, and grip strength tests. Furthermore, telmisartan or nifedipine restored myelin basic protein mRNA and protein expression and increased luxol fast blue-staining intensity. Telmisartan or nifedipine attenuated cuprizone-induced oxidative stress and apoptosis by decreasing brain malondialdehyde and caspase-3 along with restoring reduced glutathione and brain-derived neurotrophic factor levels. Telmisartan or nifedipine exerted an anti-inflammatory effect by reducing the expression of nuclear factor kappa B (NF-κB p65) as well as pro-inflammatory cytokines and elevating the expression of IκB-α. In parallel, telmisartan or nifedipine upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the levels of heme oxygenase-1 and NADPH quinone oxidoreductase 1 enzymes. In conclusion, the current study provides evidence for the protective effect of telmisartan and nifedipine in cuprizone-induced demyelination and behavioral dysfunction in mice possibly by modulating NF-κB and Nrf2 signaling pathways.