Linhui Feng,Heping Cui,Pusen Chen,Khizar Hayat,Xiaoming Zhang,Chi-Tang Ho
An Amadori rearrangement product (ARP) derived from ribose (Rib) and glutathione (GSH) was prepared and identified as N-(1-deoxy-d-ribulos-1-yl)-glutathione by ultraperformance liquid chromatography–tandem mass spectrometry and NMR. Thermal treatment of the ARP aqueous solution was conducted, and a relatively high temperature was found to accelerate the degradation of the ARP. The concentration of furans formed at 120 °C was more than 6.39 times that at 100 °C, and especially, the high temperature favored the formation of furfural and 4-hydroxy-5-methyl-3(2H)-furanone through deoxyosone dehydration. The promoting role of extra-added GSH or its constituent amino acids was investigated in the volatile formation during thermal processing of the ARP. Both, the added GSH and its constituent amino acids, could timely capture glyoxal (GO) and methylglyoxal (MGO) to facilitate Strecker degradation, which improved pyrazine formation. Compared with glycine and glutamic acid, cysteine was the most effective extra-added amino acid to react with GO and MGO to produce pyrazine and methylpyrazine. More importantly, the cysteine degraded from extra-added GSH effectively accelerated the generation of sulfur-containing volatile compounds through the reaction of cysteine degradation products with furans and shorter-chain α-dicarbonyl compounds.
Bin Wu,Ling Meng,Yan Zhao,Junjie Li,Qiuyun Tian,Yayan Pang,Chunguang Ren,Zhifang Dong
Social creatures must attend to threat signals from conspecifics and respond appropriately, both behaviorally and physiologically. In this work, we show in mice a threat-sensitive immune mechanism that orchestrates psychological processes and is amenable to social modulation. Repeated encounters with socially cued threats triggered meningeal neutrophil (MN) priming preferentially in males. MN activity was correlated with attenuated defensive responses to cues. Canonical neutrophil-specific activation marker CD177 was upregulated after social threat cueing, and its genetic ablation abrogated male behavioral phenotypes. CD177 signals favored meningeal T helper (Th)1-like immune bias, which blunted neural response to threatening stimuli by enhancing intrinsic GABAergic inhibition within the prelimbic cortex via interferon-gamma (IFN-γ). MN signaling was sensitized by negative emotional states and governed by socially dependent androgen release. This male-biased hormone/neutrophil regulatory axis is seemingly conserved in humans. Our findings provide insights into how immune responses influence behavioral threat responses, suggesting a possible neuroimmune basis of emotional regulation.
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