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Emerging evidence has implicated nicotinamide adenine dinucleotide (NAD+) metabolism in various inflammatory diseases. In the study, the role of NAD+ metabolism in Complete Freund's Adjuvant (CFA)‐evoked inflammatory pain and the underlying mechanisms are investigated. The study demonstrated that CFA induced upregulation of nicotinamide phosphoribosyltransferase (NAMPT) in dorsal root ganglia (DRG) without significant changes in the spinal cord. Inhibition of NAMPT expression by intrathecal injection of NAMPT siRNA alleviated CFA‐induced pain‐like behavior, decreased NAD+ contents in DRG, and lowered poly‐(ADP‐ribose) polymerase 1 (PARP1) activity levels. These effects are all reversed by the supplement of nicotinamide mononucleotide (NMN). Inhibition of PARP1 expression by intrathecal injection of PARP1 siRNA alleviated CFA‐induced pain‐like behavior, while elevated NAD+ levels of DRG. The analgesic effect of inhibiting NAMPT/NAD+/PARP1 axis can be attributed to the downregulation of the NF‐κB/IL‐1β inflammatory pathway. Double immunofluorescence staining showed that the expression of NAMPT/NAD+/PARP1 axis is restricted to DRG neurons. In conclusion, PARP1 activation in response to CFA stimulation, fueled by NAMPT‐derived NAD+, mediates CFA‐induced inflammatory pain through NF‐κB/IL‐1β inflammatory pathway. [ABSTRACT FROM AUTHOR]

Herein, I5+ with stereochemically active lone pairs (SCALP) was introduced into the selenate system, and two novel iodate-selenates were successfully obtained, Na7(SeO4)3(IO3) and K2(SeO4)[IO2(OH)]. Innovatively, both the title compounds are potential short-wave ultraviolet (UV) birefringent materials that possess large optical band gaps (4.57 eV and 4.27 eV, respectively) and large birefringence (0.087@546 nm and 0.101@546 nm, respectively). Simultaneously, the powder second harmonic generation (SHG) measurement reveals that Na7(SeO4)3(IO3) exhibits SHG responses of 0.6 × KDP (KH2PO4) with type-I phase matching. Detailed structural analysis and theoretical calculations confirm the excellent optical performance originating from the cooperative effect of [SeO4] and [IO3]/[IO2(OH)] functional units. This work indicates that the iodate-selenate system offers additional candidates for designing short-wave UV optical materials. [ABSTRACT FROM AUTHOR]

Emerging evidence has implicated nicotinamide adenine dinucleotide (NAD + ) metabolism in various inflammatory diseases. In the study, the role of NAD + metabolism in Complete Freund's Adjuvant (CFA)-evoked inflammatory pain and the underlying mechanisms are investigated. The study demonstrated that CFA induced upregulation of nicotinamide phosphoribosyltransferase (NAMPT) in dorsal root ganglia (DRG) without significant changes in the spinal cord. Inhibition of NAMPT expression by intrathecal injection of NAMPT siRNA alleviated CFA-induced pain-like behavior, decreased NAD + contents in DRG, and lowered poly-(ADP-ribose) polymerase 1 (PARP1) activity levels. These effects are all reversed by the supplement of nicotinamide mononucleotide (NMN). Inhibition of PARP1 expression by intrathecal injection of PARP1 siRNA alleviated CFA-induced pain-like behavior, while elevated NAD + levels of DRG. The analgesic effect of inhibiting NAMPT/NAD + /PARP1 axis can be attributed to the downregulation of the NF-κB/IL-1β inflammatory pathway. Double immunofluorescence staining showed that the expression of NAMPT/NAD + /PARP1 axis is restricted to DRG neurons. In conclusion, PARP1 activation in response to CFA stimulation, fueled by NAMPT-derived NAD + , mediates CFA-induced inflammatory pain through NF-κB/IL-1β inflammatory pathway., (© 2024 Wiley‐VCH GmbH.)

Herein, three alkali metal mercury selenites, K 2 Hg 2 (SeO 3 ) 3 , Rb 2 Hg 2 (SeO 3 ) 3 , and Cs 2 Hg 3 (SeO 3 ) 4 , were successfully obtained by a hydrothermal method. The three compounds featured same one-dimensional (1D) [HgO m (SeO 3 ) n ] ∞ chain structure that consisting of distorted Hg-O polyhedra and SeO 3 triangular pyramids with stereochemically active lone pair (SCALP) electrons. Interestingly, the rich coordination environment of Hg atoms and the size difference of alkali metal cations lead to diverse arrangement of SeO 3 groups, which makes them exhibit different birefringence. The band gaps of the three compounds indicate that they are potential ultraviolet (UV) optical materials. Detailed theoretical calculations demonstrate that the combined effects of SeO 3 triangular pyramids and Hg-O polyhedra are responsible for the optical characteristics of the reported compounds.

A novel mercury selenite sulfate named Hg 3 (SeO 3 ) 2 (SO 4 ) has been successfully synthesized under a mild hydrothermal method. Hg 3 (SeO 3 ) 2 (SO 4 ) crystallizes in a monoclinic space group P 2 1 and features a unique three-dimensional (3D) frame structure formed by [Hg 6 O 8 (SeO 3 ) 4 ] ∞ layers and SO 4 tetrahedra, which enables it to exhibit a comprehensive performance of a moderate second-harmonic generation (SHG) response of approximately 1.3 times that of baseline KH 2 PO 4 (KDP), a moderate birefringence (0.118@546 nm), and a wide band gap (4.70 eV), which indicates that it has potential for application as an ultraviolet (UV) nonlinear optical material. Detailed theoretical calculations show that the Hg 2+ -based polyhedra with large polarizability and deformability and the SeO 3 groups with stereochemically active lone pair (SCALP) electrons are the main contributors to moderate optical properties.

Nicotinamide adenine dinucleotide (NAD + ) is an omnipresent metabolite that participates in redox reactions. Multiple NAD + -consuming enzymes are implicated in numerous biological processes, including transcription, signaling, and cell survival. Multiple pieces of evidence have demonstrated that NAD + -consuming enzymes, including poly(ADP-ribose) polymerases (PARPs), sirtuins (SIRTs), and sterile alpha and TIR motif-containing 1 (SARM1), play major roles in peripheral neuropathic pain of various etiologies. These NAD + consumers primarily participate in peripheral neuropathic pain via mechanisms such as mitochondrial dysfunction, oxidative stress, and inflammation. Furthermore, NAD + synthase and nicotinamide phosphoribosyltransferase (NAMPT) have recently been found to contribute to the regulation of pain. Here, we review the evidence indicating the involvement of NAD + metabolism in the pathological mechanisms of peripheral neuropathic pain. Advanced understanding of the molecular and cellular mechanisms associated with NAD + in peripheral neuropathic pain will facilitate the development of novel treatment options for diverse types of peripheral neuropathic pain., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Authors. Published by Elsevier Ltd.. All rights reserved.)