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The increasing complexity and ubiquity of food processing and the emergence of fraudulent practices have made effective and reliable methods to authenticate food products of utmost importance. Carbohydrates, with various nutritional functions, are abundant in foods and can serve as potential markers for food authentication. However, the complex and diverse structures and properties of carbohydrates, especially polysaccharides, pose challenges. Nonetheless, significant progress has been made in this area. This paper provides an overview of the utilization of carbohydrates in food authentication since 2000, focusing on strategies involving carbohydrate-based markers, carbohydrate profiles, and carbohydrate-protein interaction-based assays. The analytical techniques, applications, challenges and limitations of these strategies are reviewed and discussed. The findings demonstrate that these strategies offer origin verification, quality assessment, adulteration detection, process control, and food species identification. Notably, oligosaccharide analysis has proven effective in food authentication and remains a promising marker, especially for analyzing intricate matrices. The advances in chromatography separation and mass spectrometry identification of isomers and trace amounts of these compounds have facilitated the discovery of such markers. In conclusion, carbohydrate analysis can play a crucial role in food authentication. Future research and development will make the authentication of carbohydrate-rich foods ever more accurate and efficient. • Carbohydrates can effectively serve as markers in authentication of food rich in carbohydrates. • Advances in chromatography, MS, and derivatization techniques addressed carbohydrate analysis challenges • The use of oligosaccharide-based approaches has demonstrated efficiency in food authentication. [ABSTRACT FROM AUTHOR]

This study tested the hypothesis that antinociceptive effects of galanin and its receptors in nucleus accumbens (NAc) of rats with inflammatory pain provoked by subcutaneous injection of 0.1 ml of 2% carrageenin into the sole of the rat's left hindpaw. The hindpaw withdrawal latencies (HWLs) in response to thermal and mechanical stimulation significantly decreased in bilateral hindpaws at 3 and 4 hour after a subcutaneous injection of carrageenin. However intra-NAc injection of 2 and 3 nmol, but not 1 nmol of galanin markedly induced an increase in the HWLs in a dose-dependent way. Western blot also showed, that the expression of galanin receptor 1 (GalR1) and galanin receptor 2 (GalR2) were significantly upregulated in NAc at 3 hour after a subcutaneous injection of carrageenin. In addition, the rats were intra-NAc injected galanin, 5 min later following by intra-NAc injection of galanin receptor antagonist galantide, the galanin-induce antinociceptive effects were suppressed by galantide. The results demonstrated that galanin and its receptors might be involved in antinociception in the NAc of rats with inflammatory pain. [ABSTRACT FROM AUTHOR]

[Display omitted] • Knock-out one allele of miR-96 causes mechanical and thermal allodynia in mice. • Increased spinal Na v 1.7, 1.8, 1.9, 1.2 contributes to allodynia in miR-96 KO mice. • Intrathecal injection of Na v 1.7 or 1.8 blocker relieves allodynia of miR-96 KO mice. • Gad2::CreERT2 conditional miR-96 knockout mice phenocopies global knockout mice. • Nerve injury induces loss of miR-96 and de-repression of Na v s in GABAergic neurons. Voltage-gated sodium channels (Na v s) 1.7, 1.8, and 1.9 are predominately expressed in peripheral sensory neurons and are critical for action potential propagation in nociceptors. Unexpectedly, we found that expression of SCN9A, SCN10A, SCN11A, and SCN2A, the alpha subunit of Na v 1.7, Na v 1.8, Na v 1.9 and Na v 1.2, respectively, are up-regulated in spinal dorsal horn (SDH) neurons of miR-96 knockout mice. These mice also have de-repression of CACNA2D1/2 in DRG and display thermal and mechanical allodynia that could be attenuated by intrathecal or intraperitoneal injection of Na v 1.7 or Na v 1.8 blockers or Gabapentin. Moreover, Gad2::CreERT2 conditional miR-96 knockout mice phenocopied global knockout mice, implicating inhibitory neurons; nerve injury induced significant loss of miR-96 in SDH GABAergic and Glutamatergic neurons in mice which negatively correlated to up-regulation of Na v 1.7, Na v 1.8, Na v 1.9 and Scn2a , this dis-regulation of miR-96 and Na v s in SDH neurons contributed to neuropathic pain which can be alleviated by intrathecal injection of Na v 1.7 or Na v 1.8 blockers. In conclusion, miR-96 is required to avoid allodynia through limiting the expression of VGCCs and Na v s in DRG and Na v s in SDH in naïve and nerve injury-induced neuropathic pain mice. Our findings suggest that central nervous system penetrating Na v 1.7 and Na v 1.8 blockers may be efficacious for pain relief. [ABSTRACT FROM AUTHOR]