Ischemic stroke represents the leading cause of adult neurological disability, with no effective therapeutic strategy. Stem cell transplantation promises a new promising for treating stroke, via cell replacement and cytokines paracrine. However, due to the effect of hostile immune microenvironment, the survival and differentiation of stem cells is limited in vivo. Furthermore, the delayed inflammatory response to stroke induced secondary neurological injury. IFN-γ as pro-inflammatory cytokine has the potential to protect stem cell population during inflammatory response, as well stimulates neurogenesis of stem cells. The purpose of this study was to investigate whether co-injection of neural stem cells and IFN-γ can improve therapeutic outcomes in ischemic stroke model. In this study, we found that IFN-γ did not interfere with the proliferation of NSCs in vitro and induced levels of subsequent neuronal differentiation significantly superior to those of other four cytokines BDNF, VEGF, TGF-β, and IGF-1. Co-delivery of IFN-γ (concentration: 50 ng) enhanced the effectiveness of NSC transplantation therapy in ischemic rats. And combined IFN-γ treatment significantly increased neurogenesis in vivo, with more BrdU / DCX dual-positive cells were found in ischemic areas. Moreover, co-treatment with IFN-γ and NSCs exerted additional neurological benefits when compared with NSC transplantation alone. In conclusion, low concentration of IFN-γ can promote the functions of transplanted NSCs and facilitate theirs ability of neurological repair. Thus, our findings suggest that co-delivery of NSCs and IFN-γ without genetic modification may be an effective, simple, and novel approach for the treatment of ischemic stroke.

Human herpesvirus 6 (HHV-6) is a T-lymphtropic and neurotropic virus that can infect various types of cells. Sequential studies reported that apoptosis of glia and neurons induced by HHV-6 might act a potential trigger for some central nervous system (CNS) diseases. HHV-6 is involved in the pathogenesis of encephalitis, multiple sclerosis (MS) and fatigue syndrome. However, the mechanisms responsible for the apoptosis of infected CNS cells induced by HHV-6 are poorly understood. In this study, we investigated the cell death processes of primary human fetal astrocytes (PHFAs) during productive HHV-6A infection and the underlying mechanisms. HHV-6A can cause productive infection in primary human fetal astrocytes. Annexin V-PI staining and electron microscopic analysis indicated that HHV-6A was an inducer of apoptosis. The cell death was associated with activation of caspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP), which is known to be an important substrate for activated caspase-3. Caspase-8 and -9 were also significantly activated in HHV-6A-infected cells. Moreover, HHV-6A infection led to Bax up-regulation and Bcl-2 down-regulation. HHV-6A infection increased the release of Smac/Diablo, AIF and cytochrome c from mitochondria to cytosol, which induced apoptosis via the caspase-dependent and -independent pathways. In addition, we also found that anti-apoptotic factors such as IAPs and NF-κB decreased in HHV-6A infected PHFAs. This is the first demonstration of caspase-dependent and -independent apoptosis in HHV-6A-infected glial cells. These findings would be helpful in understanding the mechanisms of CNS diseases caused by HHV-6.

Neuropeptide Y (NPY) is a stress-modulating neuropeptide and a promising biomarker for non-invasive assessment. Herein, a sensitive electrochemical aptasensor was developed on reduced graphene oxide/gold nanoparticle (rGO/AuNP)-modified screen-printed electrodes for selective NPY detection. A methylene blue (MB)-labeled NPY-specific aptamer was immobilized on the electrode surface through Au–S chemistry, and square-wave voltammetry (SWV) was used for signal readout. The rGO/AuNP-modified interface provided high conductivity and a large effective surface area, facilitating electron transfer and probe immobilization. Under optimized conditions, the aptasensor exhibited a linear detection range of 10–10,000 pg mL⁻¹ in PBS with a low detection limit of 1.17 pg mL⁻¹ and good linearity (R² = 0.991). In addition, the sensor showed satisfactory selectivity, reproducibility, and mechanical stability. Recovery tests in artificial sweat yielded recoveries of 91.8–107.8% with relative standard deviations below 5%, demonstrating good analytical accuracy in complex matrices. Combined with an agarose-hydrogel-assisted sampling interface and a reverse-iontophoresis-compatible wearable platform, this low-cost and facile sensing strategy provides a portable proof-of-concept approach for NPY analysis in artificial sweat and shows potential for future wearable-oriented biofluid monitoring.