RESUMEN
In this work, mechanical properties of veins and membrane of dragonfly wing were studied by means of optical/electron microscopy, tensile test and nano-indentation. It indicates that veins exhibit significantly higher strength and elastic modulus, as compared with membrane. Furthermore, finite element analysis (FEA) demonstrates that the fluctuation of Von Mises stress and displacement between varying models is undermined, due to presence of the membrane, indicating higher stability. Consequently, according to FEA of varying models involving presence of membrane, the membrane in dragonfly wing not only provides the capability to fly, but also improves obviously the strength and stability of wing structure, despite of its significantly low strength and elastic modulus. It is found that based on proper biomimetic design, bioinspired rigid-flexible coupling structure exhibits superior strength and stability, as compared with conventional rigid structure, which will provide great potential to make novel, smart, and functional structures.
RESUMEN
Paclitaxel (PTX) is an anticancer drug used to treat solid tumors, but one of its common adverse effects is chemotherapy-induced peripheral neuropathy (CIPN). Currently, there is limited understanding of neuropathic pain associated with CIPN and effective treatment strategies are inadequate. Previous studies report the analgesic actions of Naringenin, a dihydroflavonoid compound, in pain. Here we observed that the anti-nociceptive action of a Naringenin derivative, Trimethoxyflavanone (Y3), was superior to Naringenin in PTX-induced pain (PIP). An intrathecal injection of Y3 (1 µg) reversed the mechanical and thermal thresholds of PIP and suppressed the PTX-induced hyper-excitability of dorsal root ganglion (DRG) neurons. PTX enhanced the expression of ionotropic purinergic receptor P2X7 (P2X7) in satellite glial cells (SGCs) and neurons in DRGs. The molecular docking simulation predicts possible interactions between Y3 and P2X7. Y3 reduced the PTX-enhanced P2X7 expression in DRGs. Electrophysiological recordings revealed that Y3 directly inhibited P2X7-mediated currents in DRG neurons of PTX-treated mice, suggesting that Y3 suppressed both expression and function of P2X7 in DRGs post-PTX administration. Y3 also reduced the production of calcitonin gene-related peptide (CGRP) in DRGs and at the spinal dorsal horn. Additionally, Y3 suppressed the PTX-enhanced infiltration of Iba1-positive macrophage-like cells in DRGs and overactivation of spinal astrocytes and microglia. Therefore, our results indicate that Y3 attenuates PIP via inhibiting P2X7 function, CGRP production, DRG neuron sensitization, and abnormal spinal glial activation. Our study implies that Y3 could be a promising drug candidate against CIPN-associated pain and neurotoxicity.