Development of PVA/Chitosan-g-Poly (N-vinyl imidazole)/TiO2/curcumin nanofibers as high-performance wound dressing.

In this study, electrospun Poly(vinyl alcohol)/Chitosan-g-Poly (N-vinyl imidazole) (PVA/CS-g-PNVIM) wound dressing containing Titanium dioxide/Curcumin (CUR) was prepared as a novel wound healing system with multifunctional properties, including wound closure, drug release, and antibacterial activity. The wound dressing nanofibers system's mechanical, structural, and biological properties were investigated using tensile testing, degradation, X-ray diffraction, Scanning electron microscopy, Fourier transformed infrared spectroscopy, drug release, and in vivo studies. The nanofiber dressing showed excellent mechanical and hydrolytic degradation stability. CS-g-PNVIM-based nanofibers showed excellent antibacterial activity against both Escherichia coli and Staphylococcus aureus in just 1 h with 90 % growth inhibition, with no cytotoxicity to normal fibroblast cells. The animal studies showed that the wound healing and tissue regeneration process by CS-g-PNVIM-based nanofibers were faster than the control group and was completed in 14 days. In conclusion, the CS-g-PNVIM-based nanofibers are potentially promising for biocompatible antibacterial wound dressing applications with proper exudate absorption.

Spinal p38beta isoform mediates tissue injury-induced hyperalgesia and spinal sensitization.

Antagonist studies show that spinal p38 mitogen-activated protein kinase plays a crucial role in spinal sensitization. However, there are two p38 isoforms found in spinal cord and the relative contribution of these two to hyperalgesia is not known. Here we demonstrate that the isoforms are distinctly expressed in spinal dorsal horn: p38alpha in neurons and p38beta in microglia. In lieu of isoform selective inhibitors, we examined the functional role of these two individual isoforms in nociception by using intrathecal isoform-specific antisense oligonucleotides to selectively block the expression of the respective isoform. In these rats, down-regulation of spinal p38beta, but not p38alpha, prevented nocifensive flinching evoked by intraplantar injection of formalin and hyperalgesia induced by activation of spinal neurokinin-1 receptors through intrathecal injection of substance P. Both intraplantar formalin and intrathecal substance P produced an increase in spinal p38 phosphorylation and this phosphorylation (activation) was prevented when spinal p38beta, but not p38alpha, was down-regulated. Thus, spinal p38beta, probably in microglia, plays a significant role in spinal nociceptive processing and represents a potential target for pain therapy.