Novel brain-targeted nanomicelles for anti-glioma therapy mediated by the ApoE-enriched protein corona in vivo.

Background: The interactions between nanoparticles (NPs) and plasma proteins form a protein corona around NPs after entering the biological environment, which provides new biological properties to NPs and mediates their interactions with cells and biological barriers. Given the inevitable interactions, we regard nanoparticle‒protein interactions as a tool for designing protein corona-mediated drug delivery systems. Herein, we demonstrate the successful application of protein corona-mediated brain-targeted nanomicelles in the treatment of glioma, loading them with paclitaxel (PTX), and decorating them with amyloid β-protein (Aβ)-CN peptide (PTX/Aβ-CN-PMs).

Aggravated chronic brain injury after focal cerebral ischemia in aquaporin-4-deficient mice.

The water channel aquaporin-4 (AQP4) is important in brain water homeostasis, and is also involved in astrocyte growth and glial scar formation. It has been reported that AQP4 deficiency attenuates acute ischemic brain injury as a result of reducing cytotoxic edema. Here, we determined whether AQP4 deficiency influences chronic brain injury after focal cerebral ischemia induced by 30 min of middle cerebral artery occlusion (MCAO).

Antibacterial activity and cytotoxicity of two novel cross-linking antibacterial monomers on oral pathogens.

Objectives: The antibacterial activity and cytotoxicity of two novel cross-linking antibacterial monomers, 2-methacryloxylethyl dodecyl methyl ammonium bromide (MAE-DB) and 2-methacryloxylethyl hexadecyl methyl ammonium bromide (MAE-HB) were tested in this study.

Design: The minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of unpolymerized MAE-DB and MAE-HB against eight strains of oral bacteria were tested using a broth dilution test. Time-kill determinations were performed to examine the kinetics of unpolymerized MAE-DB and MAE-HB against Streptococcus mutans UA159 and Streptococcus sanguinis ATCC6715.

CysLT2 receptor-mediated AQP4 up-regulation is involved in ischemic-like injury through activation of ERK and p38 MAPK in rat astrocytes.

Aims: We previously reported that cysteinyl leukotriene receptor 2 (CysLT(2)) mediates ischemic astrocyte injury, and leukotriene D(4)-activated CysLT(2) receptor up-regulates the water channel aquaporin 4 (AQP4). Here we investigated the mechanism underlying CysLT(2) receptor-mediated ischemic astrocyte injury induced by 4-h oxygen-glucose deprivation and 24-h recovery (OGD/R).

Main Methods: Primary cultures of rat astrocytes were treated by OGD/R to construct the cell injury model.

Baicalin attenuates oxygen-glucose deprivation-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase activation in PC12 cells.

Aim: To determine whether the flavonoid baicalin attenuates oxygen-glucose deprivation (OGD)-induced injury by inhibiting oxidative stress-mediated 5-lipoxygenase (5-LOX) activation in PC12 cells.

Methods: The effects of baicalin and the 5-LOX inhibitor zileuton on the changes induced by OGD/recovery or H(2)O(2) (an exogenous reactive oxygen species [ROS]) in green fluorescent protein-5-LOX-transfected PC12 cells were compared.

Results: Both baicalin and zileuton attenuated OGD/recovery- and H(2)O(2)-induced injury and inhibited OGD/recovery-induced production of 5-LOX metabolites (cysteinyl leukotrienes) in a concentration-dependent manner.

[Preparation and identification of polyclonal antibody against cysteinyl leukotriene receptor 2].

Objective: To prepare and identify a polyclonal antibody against cysteinyl leukotriene receptor (CysLT(2)receptor).

Methods: Rabbits were immunized with KLH-coupled CysLT(2) receptor peptide to prepare the polyclonal antibody (pAb). The titer of the pAb in rabbit plasma was detected by indirect ELISA, and the specificity of the pAb was tested by antigen blockade.

[Preparation and identification of a polyclonal antibody against novel cysteinyl leukotriene receptor GPR17].

Objective: To prepare and identify a polyclonal antibody (pAb) against GPR17, a novel cysteinyl leukotriene receptor.

Methods: Rabbits were immunized with KLH-coupled GPR17 peptide to prepare the pAb. The titer of the pAb in rabbit plasma was detected by indirect ELISA, and the specificity of the pAb was tested by antigen blockade.

Oxygen-glucose deprivation activates 5-lipoxygenase mediated by oxidative stress through the p38 mitogen-activated protein kinase pathway in PC12 cells.

5-Lipoxygenase (5-LOX) is a key enzyme catalyzing arachidonic acid to form leukotrienes. We have reported that ischemic-like injury activates 5-LOX in PC12 cells; however, the mechanisms are unknown. To determine whether ischemic-like injury activates 5-LOX mediated by oxidative stress through the p38 MAPK pathway, we transfected GFP-5-LOX into PC12 cells and induced ischemic-like injury by oxygen-glucose deprivation (OGD).