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Current in vivo Models for Brain Disorders
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Marta Guerra-Rebollo, Cristina Garrido
Nanotechnology has also offered the first rays of hope in the treatment for neuroAIDS, which until the date has no effective vaccines or specific drug therapy. Dou et al. have developed a macrophage-based NP platform for antiretroviral drug delivery [36]. They designed a novel bone marrow-derived macrophage (BMM) pharmacologic NP delivery system. Hypothesising that the system will improve drug distribution to areas of active viral replication, and extend dosing intervals and this way achieving therapeutic efficacy. Their model was based on loading indinavir (antiretroviral drug) nanosuspension into BMMs (NP-IDV-BMMs) and administered intravenously into naive mice or NOD/SCID mice humanised with human peripheral blood lymphocytes reconstitution infected with human immunodeficiency virus 1 (HIV-1). Cell tissue distribution was tracked by single-photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI) of radio- and superparamagnetic iron oxide (SPIO; Feridex)-labelled BMMs, and confirmed by histology. Antiretroviral therapeutic responses and immune response were studied in humanised infected mice.
Poria cocos polysaccharide decorated selenium nanoparticles attenuate colitis by suppressing hyper inflammation
Published in Gary Bañuelos, Zhi-Qing Lin, Dongli Liang, Xue-bin Yin, Selenium Research for Environment and Human Health: Perspectives, Technologies and Advancements, 2019
H. Yang, Y.F. Yang, L.Q. Duan, Q.J. Ling, Z. Huang*
As shown in Figure 1a, the particle-size distribution of PYN-SeNPs was 35–80 nm, which is smaller compared to 305–900 nm of SeNPs. The dispersity of PYN-SeNPs is also better than SeNPs itself (Fig. 1b). The cellular uptake of PYN-SeNPs in Bone Marrow Derived Macrophage (BMDM) was in a time-dependent manner, and BMDM macrophages uptake much more PYN–SeNPs than PYN.
The cationic (calcium and lead) and enzyme conundrum
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Jane Kasten-Jolly, David A. Lawrence
A study of phosphorylation of erythrocyte membrane proteins after in vitro Pb exposure suggested involvement of PKC, since membrane protein phosphorylation was not detected after Pb treatment of PKC-depleted erythrocytes (Belloni-Olivi et al. 1996). Rodent bone marrow derived macrophages cultured in the presence of Pb and endotoxin released 10-fold more IL-6, TNFα, IL-12, and PGE(2), but released a reduced amount of IL-10 compared to cells cultured in the presence of endotoxin alone (Flohe et al. 2002). Inhibition of PKC blocked the increase in IL-6 and TNFα secretion. It was concluded that Pb ions primed the macrophages to enhance proinflammatory cytokine secretion and that this elevation was due to activation of PKC. Deng and Poretz (2002) examined the effect of Pb exposure on oligodendrocyte progenitor cells (OPCs) and noted that Pb concentrations ≥5–10 µM were cytotoxic to the cells within 24 hr, but 1 µM Pb inhibited proliferation and differentiation of the OPCs through activation of PKC as determined by inhibitors and promotors of PKC activity. Exposure to Pb promoted translocation of PKC from the cytoplasm to the membrane of the cells. It was concluded that 1 µM Pb exposure inhibited proliferation and differentiation of the OPCs through a mechanism requiring PKC activation likely through binding of DAG.