Journal of Agricultural and Food Chemistry最新文献

This research investigates how phlorizin, a plant-derived dihydrochalcone, modulates glutamate release in synaptosomes and exerts neuroprotective effects in a rat model of kainic acid (KA)-induced excitotoxicity. In rat cortical synaptosomes, phlorizin concentration-dependently inhibited evoked glutamate release (IC₅₀ = 14.4 μM). This effect was abolished under calcium-free conditions or by blockade of P/Q type but not N type Ca²⁺ channels. In vivo, oral phlorizin pretreatment (100 mg/kg/day, 7 days) attenuated KA-induced seizures and neurodegeneration, restored NeuN and GAP-43 expression, and normalized cortical glutamate homeostasis by regulating GLT-1, glutamine synthetase, SNAT1/3, glutaminase, and VGLUT1. It shifted NMDA receptor subunit composition toward a neuroprotective profile (increasing GluN2A/GluN2B ratio) and suppressed astrocytic IL-1β/IL-1R1/Src signaling. Furthermore, phlorizin preserved blood brain barrier integrity by increasing ZO-1 and reducing albumin extravasation and MMP-9. These results demonstrate that phlorizin exerts multifaceted neuroprotection by inhibiting synaptic glutamate release, modulating glutamate homeostasis, and suppressing neuroinflammation and barrier disruption.

Research to date has focused on understanding the hormonal and genetic factors regulating the transition from physiologically mature to ripe fruit. Knowledge of factors regulating the time from anthesis to fruit maturity, where the seed coat turns black and fruit becomes competent to ripen, is limited. Accumulations of nonstructural carbohydrates, organic acids, and phytohormones were profiled during fruit development of two kiwiberry (Actinidia arguta) genotypes with contrasting maturation times over two seasons. Seed maturation and rise in nonstructural carbohydrates were associated with salicylic acid (SA), abscisic acid, and their metabolites in fruit of the “Early” but not the “Late” maturing genotype. As identification of dynamic gene–metabolite interactions over time is challenging, three data integration frameworks (TimeOmics, MOFA, and MINT) were used to interrogate “omics” data and found to be complementary. SA-associated genes related to plant defense and immunity were identified as having a novel function in kiwiberry development, by promoting fruit maturation.

Gigantol, a naturally active molecule derived from the edible plant Dendrobium, has been demonstrated to have hepatoprotective potential, but its effect in the treatment of metabolic dysfunction-associated steatohepatitis (MASH) remains unclear. Here, we found that gigantol treatment greatly corrected dyslipidemia, hepatic dysfunction, and hepatic histological changes that arrested MASH occurrence in high-fat and high-fructose-diet (HFFD)-fed mice. Mechanistically, gigantol promoted the nuclear translocation of the transcription factor EB (TFEB) to regulate the key factors of lipophagy and fatty acid oxidation to maintain hepatic lipid metabolism homeostasis. Consistent results were observed in palmitic acid-induced cell models. Notably, silencing TFEB reversed the effect of gigantol in enhancing lipophagy and fatty acid oxidation in vivo and in vitro. In summary, this study provides strong evidence to demonstrate that gigantol attenuates HFFD-induced MASH by promoting TFEB-dependent lipophagy and fatty acid oxidation, suggesting that gigantol, an edible plant-derived compound, is promising to be developed as a therapeutic drug for MASH in the future.

Neuroinflammation can be brought on by intestinal inflammatory agents and metabolites generated by the gut microbiota that can pass across the blood–brain barrier. Taraxacum coreanum is rich in the bioactive compound luteolin (LT), a molecule known for its potent antioxidant and anti-inflammatory activities. The current research investigated whether LT prevents inflammatory responses and barrier dysfunction in the brain and gut of lipopolysaccharide (LPS)-injected mice. LT (10 and 20 mg/kg/day) effectively lowered the brain levels of pro-inflammatory mediators and cytokines triggered by LPS stimulation. Moreover, occludin and ZO-1 are two tight junction proteins whose expression was markedly elevated by LT. In the intestine, LT not only attenuated the levels of inflammatory mediators but also markedly upregulated tight junction protein expression relative to the LPS-treated group. LT markedly reversed LPS-induced dysbiosis by increasing beneficial taxa such as Bacteroidota, Actinobacteriota, Murivaculaceae, and Lactobacillus. In addition, LT reduced the relative abundance of Firmicutes and Desulfovibrio. Collectively, LT from Taraxacum coreanum may attenuate neuroinflammation and maintain blood–brain barrier integrity by suppressing inflammatory responses, protecting the gut barrier, and modulating the gut microbiome.

With the consumer pursuit for natural antioxidants, astaxanthin production by Xanthophyllomyces dendrorhous has garnered significant interest. However, the limited production levels hinder the industrial application of astaxanthin. This study systematically examined the effects of metabolic regulators including metal ions, surfactants, and vegetable oils on the astaxanthin synthesis by X. dendrorhous LX6. Transcriptome analysis found that genes of crtYB and crtI for astaxanthin synthesis, adhp, acat, and fadD for lipid metabolism, and pla2g7 for cell membrane synthesis played major roles in the regulation of astaxanthin synthesis after the supplementation of metabolic regulators. Lipidomics analysis showed that the supplementation of Tween 80 or corn oil can regulate the fluidity of the cell membrane, affecting the astaxanthin production. Ultimately, X. dendrorhous LX6 synthesized 714.7 mg/L of astaxanthin using wheat straw hydrolysate as the substrate under the optimized conditions with the astaxanthin content of 18 mg/g, offering valuable insights for the industrial application of X. dendrorhous.