The Fate of SWCNTs in Mouse Peritoneal Macrophages: Exocytosis, Biodegradation, and Sustainable Retention.

The understanding of toxicological and pharmacological profiles of nanomaterials is an important step for the development and clinical application of nanomedicines. Carbon nanotubes (CNTs) have been extensively explored as a nanomedicine agent in pharmaceutical/biomedical applications, such as drug delivery, bioimaging, and tissue engineering. The biological durability of CNTs could affect the function of CNTs-based nanomedicines as well as their toxicity in cells and tissues. Therefore, it is crucial to assess the fate of nanomedicine in phagocytes. Herein, we investigated the candidate fate of acid-oxidized single-walled carbon nanotubes (SWNCTs) in non-activated primary mouse peritoneal macrophages (PMQ). The sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results showed that the intracellular SWCNTs continued growing from 4 to 36 h in PMQ. After replacing the exposure medium, we found the exosome induced by SWCNTs on the surface of macrophages according to scanning electron microscope (SEM) observation. The near-infrared (NIR) absorption increase of the supernatant samples after post-exposure indicates that SWCNTs exocytosis occurred in PMQ. The decreasing intracellular SWCNTs amount suggested the incomplete biodegradation in PMQ, which was confirmed by Raman spectroscopy and transmission electron microscopy (TEM). The combined data reveal that SWCNTs could be retained for more than 60 h in macrophages. Then sustainable retention of SWCNTs in primary macrophages was coexist with exocytosis and biodegradation. The findings of this work will shed light on the bioimaging, diagnosis and other biomedical applications of CNTs-based nanomedicines.

Gene expression profiling analysis of locus coeruleus in idiopathic Parkinson's disease by bioinformatics.

This study aimed to explore the underlying molecular mechanisms of idiopathic Parkinson's disease (IPD) by bioinformatics analysis. Gene expression profile GSE34516 was downloaded from the Gene Expression Omnibus. Eight locus coeruleus post-mortem tissue samples derived from four IPD patients and four neurological healthy controls were used to identify the differentially expressed genes (DEGs) by paired t test. Based on the DEGs, principal components were analyzed. The Gene Ontology functional and Kyoto Encyclopedia of Genes and Genomes pathway analysis of the genome microarray data were then performed. Finally, protein-protein interaction (PPI) network of the DEGs was constructed. Total 261 DEGs including 195 up-regulated and 66 down-regulated DEGs were identified. Intracellular protein transport and RNA splicing via transesterification reactions were selected as the most two significantly enriched functions. Mismatch repair, N-glycan biosynthesis, spliceosome and nucleotide excision repair were the significantly enriched pathways. In the PPI network, CTSS, CD53, IGSF6, PTPRC and LAPTM5 were the hub nodes. Intracellular protein transport and RNA splicing via transesterification reactions were closely associated with IPD. The DEGs, such as CX3CR1, SLC5A7, CD53 and PTPRC may be the potential targets for IPD diagnosis and treatment.

Triptolide treatment reduces Alzheimer's disease (AD)-like pathology through inhibition of BACE1 in a transgenic mouse model of AD.

The complex pathogenesis of Alzheimer's disease (AD) involves multiple contributing factors, including amyloid ß (Aß) peptide accumulation, inflammation and oxidative stress. Effective therapeutic strategies for AD are still urgently needed. Triptolide is the major active compound extracted from Tripterygium wilfordii Hook.f., a traditional Chinese medicinal herb that is commonly used to treat inflammatory diseases. The 5-month-old 5XFAD mice, which carry five familial AD mutations in the ß-amyloid precursor protein (APP) and presenilin-1 (PS1) genes, were treated with triptolide for 8 weeks. We observed enhanced spatial learning performances, and attenuated Aß production and deposition in the brain. Triptolide also inhibited the processing of amyloidogenic APP, as well as the expression of ßAPP-cleaving enzyme-1 (BACE1) both in vivo and in vitro. In addition, triptolide exerted anti-inflammatory and anti-oxidative effects on the transgenic mouse brain. Triptolide therefore confers protection against the effects of AD in our mouse model and is emerging as a promising therapeutic candidate drug for AD.

Properties of rosin-based waterborne polyurethanes/cellulose nanocrystals composites.

Polymers from renewable biomass are viable supplements for synthetic polymers. In this study, cellulose nanocrystals (CNs) were used as nanofillers to improve properties of rosin-based waterborne polyurethanes (RWPU). The morphology, structure, thermal, and mechanical properties of the RWPU/CNs nanocomposites were investigated. It demonstrated that CNs were compatible with RWPU and dispersed homogeneously in the polymer matrix. CNs as nanofillers improved tensile strength of RWPU significantly. Tensile strength of RWPU/CNs composite films increased from 28.2 to 52.3 MPa with increasing CNs amount from 0 to 20 wt%. Moreover, the thermal stability of RWPU was also improved by CNs and the glass transition temperature of RWPU/CNs decreased comparing with RWPU. This work provided a novel pathway for preparation of biomass-based WPU with excellent properties from cellulose and rosin.

[Effect of puerarin in myocardial protection in rats with acute and chronic alcoholism].

OBJECTIVE: To investigate the protective effect of puerarin on the myocardium of rats with acute and chronic alcoholism. METHODS: In acute alcoholism experiment, normal male SD rats were randomly divided into the control group, alcoholism group and puerarin group (n=8), and high- and low-dose puerarin was administered. In chronic alcoholism experiment, increasing puerarin doses were given. Serum and myocardial levels of spartate aminotransferase (AST) and creatine phosphokinase (CPK) were determined using enzymatic methed, and superoxide dismutase (SOD), malondialdehyde (MDA), Ca(2+)-Mg(2+)-ATPase, and Na(+)-K(+)-ATPase in the myocardium were assayed with colorimetric method. HE staining was used to observe the microscopic changes of the myocardium. RESULTS: Compared with alcoholism group, puerarin-treated groups showed significantly lowered myocardial contents of MDA, CPK and AST and serum levels of AST and CPK (P<0.05, P<0.01) and increased myocardial SOD (P<0.05, P<0.01), Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase activity (P<0.05, P<0.01), but Na(+)-K(+)-ATPase was similar between the two groups (P>0.05). HE staining of the myocardium showed cell swelling and obscure cell boundaries in alcoholism group, especially in chronic alcoholism group. The myocardial structure in puerarin group remained clear and regular. CONCLUSION: Puerarin can protect from myocardial injuries induced by acute and chronic alcoholism in rats.