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BackgroundDespite accumulating evidence on the role of glial cells and their associated chemicals in mechanisms of pain, few studies have addressed the potential role of chemokines in the descending facilitation of chronic pain. We aimed to study the hypothesis that CXCL1/CXCR2 axis in the periaqueductal gray (PAG), a co-restructure of the descending nociceptive system, is involved in descending pain facilitation.MethodsIntramedullary injection of Walker 256 mammary gland carcinoma cells of adult female Sprague Dawley rats was used to establish a bone cancer pain (BCP) model. RT-PCR, Western blot, and immunohistochemistry were performed to detect pNfkb, Cxcl1, and Cxcr2 and their protein expression in the ventrolateral PAG (vlPAG). Immunohistochemical co-staining with NeuN, GFAP, and CD11 were used to examine the cellular location of pNFκB, CXCL1, and CXCR2. The effects of NFκB and CXCR2 antagonists and CXCL1 neutralizing antibody on pain hypersensitivity were evaluated by behavioral testing.ResultsBCP induced cortical bone damage and persistent mechanical allodynia and increased the expression of pNFκB, CXCL1, and CXCR2 in vlPAG. The induced phosphorylation of NFκB was co-localized with GFAP and NeuN, but not with CD11. Micro-injection of BAY11-7082 attenuated BCP and reduced CXCL1 increase in the spinal cord. The expression level of CXCL1 in vlPAG showed co-localization with GFAP, but not with CD11 and NeuN. Micro-administration of CXCL1 neutralizing antibody from 6 to 9 days after inoculation attenuated mechanical allodynia. Furthermore, vlPAG application of CXCL1 elicited pain hypersensitivity in normal rats. Interestingly, CXCR2 was upregulated in vlPAG neurons (not with CD11 and GFAP) after BCP. CXCR2 antagonist SB225002 completely blocked the CXCL1-induced mechanical allodynia and attenuated BCP-induced pain hypersensitivity.ConclusionThe NFκB-dependent CXCL1-CXCR2 signaling cascade played a role in glial-neuron interactions and in descending facilitation of BCP.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1391-2) contains supplementary material, which is available to authorized users.

While great progress has been achieved in all-polymer solar cells (all-PSCs), the efficiency of all-PSCs is primarily limited by polymer acceptors that lack a high extinction coefficient, high electron mobility, and good compatibility with polymer donors. Here we designed and developed a polymer acceptor PFA1 based on a nonfullerene acceptor framework with a fluorine substituent on the 1,1-dicyanomethylene-3-indanone unit. In combination with an electron-donating polymer, PTzBI-oF, the blend film presents an extended and intensified absorption profile, enhanced electron mobility, and favorable film morphology. The optimized all-PSCs exhibit a remarkably high efficiency of 15.11%, which is, to the best of our knowledge, the highest performance yet reported for an all-PSC. Of particular importance is the applicability of PFA1 as a universal polymer acceptor with a range of polymer donors to achieve impressively high efficiencies. These properties enable a new molecular design strategy for the construction of polymer acceptors toward applications in high-performance all-PSCs.

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Single-wall carbon nanotube/polyaniline (SWCNT/PANI) and graphene sheet/polyaniline (GS/PANI) composites were prepared by a simple alcohol-assisted dispersion and pressing process. The SWCNTs and GSs were synthesized by the dc arc-discharge method. The dc electrical conductivity and the electromagnetic interference (EMI) shielding effectiveness (SE) of these two kinds of composites were measured. The experimental results reveal that the conductivity and the EMI SE of the GS/PANI composite are better than that of the SWCNT/PANI composite, and the absorption proportion of the SWCNT/PANI composite is higher than that of the GS/PANI composite. The EMI shielding results (2–18 GHz) also show that both composites present an absorption-dominant mechanism and present a wide application prospect in the field of EMI shielding and microwave absorption.