RESUMO
Si-based electrodes offer exceptionally high capacity and energy density for lithium-ion batteries (LIBs),but suffer from poor structural stability and electrical conductivity that hamper their practical applications. To tackle these obstacles, we design a C/polymer bilayer coating deposited on Si-SiOx microparticles. The inner C coating is used to improve electrical conductivity. The outer C-nanoparticle-reinforced polypyrrole (CNP-PPy) is a polymer matrix composite that can minimize the volumetric expansion of Si-SiOx and enhance its structural stability during battery operation. Electrodes made of such robust Si-SiOx@C/CNP-PPy microparticles exhibit excellent cycling performance: 83% capacity retention (794 mAh g-1) at a 2 C rate after more than 900 cycles for a coin-type half cell, and 80% capacity retention (with initial energy density of 308 Wh kg-1) after over 1100 cycles for a pouch-type full cell. By comparing the samples with different coatings, an in-depth understanding of the performance enhancement is achieved, i.e., the C/CNP-PPy with cross-link bondings formed in the bilayer coating plays a key role for the improved structural stability. Moreover, a full battery using the Si-SiOx@C/CNP-PPy electrode successfully drives a car model, demonstrating a bright application prospect of the C/polymer bilayer coating strategy to make future commercial LIBs with high stability and energy density.
RESUMO
BACKGROUND: Intervertebral disc (IVD) degeneration is a condition characterized by a reduction in the water and extracellular matrix content of the nucleus pulposus (NP) and is considered as one of the dominating contributing factors to low back pain. Recent evidence suggests that stromal cell-derived factor 1α (SDF-1α) and its receptor C-X-C chemokine receptor type 4 (CXCR4) direct the migration of stem cells associated with injury repair in different musculoskeletal tissues. AIM: To investigate the effects of SDF-1α on recruitment and chondrogenic differentiation of nucleus pulposus-derived stem cells (NPSCs). METHODS: We performed real-time RT-PCR and enzyme-linked immunosorbent assay to examine the expression of SDF-1α in nucleus pulposus cells after treatment with pro-inflammatory cytokines in vitro. An animal model of IVD degeneration was established using annular fibrosus puncture in rat coccygeal discs. Tissue samples were collected from normal control and degeneration groups. Differences in the expression of SDF-1α between the normal and degenerative IVDs were analyzed by immunohistochemistry. The migration capacity of NPSCs induced by SDF-1α was evaluated using wound healing and transwell migration assays. To determine the effect of SDF-1α on chondrogenic differentiation of NPSCs, we conducted cell micromass culture and examined the expression levels of Sox-9, aggrecan, and collagen II. Moreover, the roles of SDF-1/CXCR4 axis in the migration and chondrogenesis differentiation of NPSCs were analyzed by immunofluorescence, immunoblotting, and real-time RT-PCR. RESULTS: SDF-1α was significantly upregulated in the native IVD cells cultured in vitro with pro-inflammatory cytokines, such as interleukin-1ß and tumor necrosis factor-α, mimicking the degenerative settings. Immunohistochemical staining showed that the level of SDF-1α was also significantly higher in the degenerative group than in the normal group. SDF-1α enhanced the migration capacity of NPSCs in a dose-dependent manner. In addition, SDF-1α induced chondrogenic differentiation of NPSCs, as evidenced by the increased expression of chondrogenic markers using histological and immunoblotting analyses. Real-time RT-PCR, immunoblotting, and immunofluorescence showed that SDF-1α not only increased CXCR4 expression but also stimulated translocation of CXCR4 from the cytoplasm to membrane, accompanied by cytoskeletal rearrangement. Furthermore, blocking CXCR4 with AMD3100 effectively suppressed the SDF-1α-induced migration and differentiation capacities of NPSCs. CONCLUSION: These findings demonstrate that SDF-1α has the potential to enhance recruitment and chondrogenic differentiation of NPSCs via SDF-1/CXCR4 chemotaxis signals that contribute to IVD regeneration.