Journal of Agricultural and Food Chemistry最新文献

Rice lesion mimic mutants (LMMs) spontaneously form lesion-like symptoms without pathogen infection and are vital for studying plant immune and defense responses. Here, we identified an EMS-mutagenized Nipponbare-derived LMM, russet spots leaf (rsp), exhibiting leaf russet spots and deteriorated agronomic traits with significantly reduced grain yield. These abnormal phenotypes correlate with impaired photosynthetic efficiency, aberrant programmed cell death (PCD) and excessive reactive oxygen species (ROS) accumulation. Moreover, rsp shows enhanced resistance to bacterial blight and rice stripe virus, driven by altered defense-related genes and metabolites. Map-based cloning localized RSP (encoding MED subunit 33a), where a single nucleotide substitution causes its inactivation. This mutation alters plant responses to abiotic stresses and exogenous hormones, likely via disrupting its conserved domain mediating multiple biological processes. Our findings confirm RSP as a pivotal regulator of immune responses and grain yield, laying a theoretical foundation for breeding high-yield, high-quality and disease-resistant rice cultivars.

NAFLD-related hepatic steatosis is a growing global health concern. We developed food-grade gliadin hydrolysate-berberine-chitosan nanoparticles (BBR-NPs) and evaluated their bioactivity in oleic acid-challenged HepG2 cells and high-fat diet (HFD)-fed mice. In vitro, BBR-NPs reduced triglycerides, total cholesterol, and LDL-C, increased HDL-C, and alleviated oxidative stress by decreasing ROS and malondialdehyde while enhancing superoxide dismutase activity. In vivo, oral BBR-NPs attenuated hepatic lipid deposition and improved serum/hepatic lipid indices, ALT/AST, oxidative stress markers, insulin resistance, and inflammatory cytokines, with generally more pronounced effects than free berberine at the same nominal dose in this model. Integrated hepatic metabolomics and transcriptomics suggested coordinated regulation of lipid homeostasis, including fatty acid oxidation, de novo lipogenesis, and cholesterol/bile acid metabolism. Collectively, BBR-NPs represent a scalable oral delivery approach that may enhance berberine's metabolic benefits in diet-induced steatosis; however, pharmacokinetic and tissue exposure studies are needed to confirm formulation-specific advantages.

Low temperature has a serious effect on Actinidia arguta growth and development. However, the mechanisms of how MYB proteins participate in freezing stress in A. arguta are still unclear. In this study, AaMYB16 was transformed into Arabidopsis thaliana and A. arguta. The relevant physiological and biochemical indexes were determined, and the regulatory model of AaMYB16 was preliminarily discussed. The results showed that there was an interaction between AaMYB16 and AabHLH137. AabHLH18 and AabHLH137 played a role in the upstream of AaMYB16. Overexpress AaMYB16 increased plant susceptibility to freezing stress, whereas silencing AaMYB16 enhanced freezing tolerance in A. arguta. Our results suggest that AaMYB16 is a negative regulator of freeze response in A. arguta. The AabHLH18/AabHLH137-AaMYB16 module plays an important role in freezing stress. These results provide insights into the molecular mechanism of low-temperature regulation of A. arguta, and a theoretical basis for fruit storage and breeding of A. arguta.

Emerging research evidence has established the critical role of inflammatory cascades in the development and progression of alcoholic liver injury with hepatocellular death serving as a principal driver. Notably, the dysregulated interplay between mitochondrial homeostasis and pyroptosis is primarily responsible for the alcohol-induced aberrant liver immune microenvironment, characterized by nonresolving inflammation. Given the considerable limitations in the current treatment for alcoholic steatohepatitis (ASH), it is imperative to explore targeted nutritional interventions as alternative therapies. Here, we established an ASH model with C57BL/6J mice and demonstrated that astaxanthin (AST) administration significantly protected against alcohol-induced inflammatory liver injury through dual mechanisms: 1) suppression of hepatocyte pyroptosis by inhibiting the NLRP-3/Caspase/GSDMD signaling axis and 2) mitigation of mitochondrial dysfunction evidenced by structural membrane integrity restoration and redox homeostasis rebalancing. Mechanistically, AST intervention impeded the cytoplasmic translocation of mitochondrial DNA (mtDNA), thereby concurrently inhibiting AIM2 inflammasome activation and cGAS/STING signaling. In vitro studies further confirmed dose-dependent attenuation of alcohol-induced hepatotoxicity by AST, marked by reduced pyroptotic cell death and diminished proinflammatory cytokine secretion (IL-1β, IL-18). Mitochondrial protection was further evidenced through restored membrane potential (ΔΨm), decreased cytoplasmic Cytochrome C release, and attenuated mtDNA leakage. Moreover, we identified a novel molecular interaction, wherein AST competitively binds lipid-binding motifs within the β1-β2 loop of the GSDMD-N-terminal domain, potentially interfering with pyroptotic pore formation. Further overexpression experiments confirmed the improvement effect of AST on pyroptosis induced by GSDMD-N pore formation. Concurrently, AST exhibited potent antioxidant effects against alcohol-induced cardiolipin peroxidation, suggesting dual therapeutic modalities targeting both pyroptotic execution and mitochondrial membrane stabilization. Collectively, our findings identify AST as a promising candidate for therapeutic interventions against alcoholic inflammatory liver injury through coordinated modulation of the pyroptosis-mitochondrial homeostasis crosstalk, offering novel insights into nutritional intervention strategies for alcohol-related liver pathologies.