Protein lysine lactylation is a new post-translational modification (PTM) prevalently found in fungi and mammalian cells that directly stimulates gene transcription and regulates the glycolytic flux. However, lysine lactylation sites and regulations remain largely unexplored, especially in cereal crops. Herein, we report the first global lactylome profile in rice, which effectively identified 638 lysine lactylation sites across 342 proteins in rice grains. Functional annotations demonstrated that lysine lactylation was enriched in proteins associated with central carbon metabolism and protein biosynthesis. We also observed that proteins serving as nutrition reservoirs in rice grains were frequently targeted by lactylation. Homology analyses indicated that lactylation was conserved on both histone and nonhistone proteins across plants, human cells, and fungi. In addition to lactylation, additional types of acylations could co-occur in many proteins at identical lysine residues, indicating potential cross-talks between these modifications. Our study provided a comprehensive profile of protein lysine lactylation in cereal crop grains.

The proportion of foodborne disease caused by pathogenic microorganisms is rising worldwide, with staphylococcal food poisoning being one of the main causes of this increase. Juglone is a plant-derived 1,4-naphthoquinone with confirmed antibacterial and antitumor activities. However, the specific mechanism underlying its antibacterial activity against Staphylococcus aureus remains unclear. To elucidate the mechanism underlying its antibacterial activity, isobaric tags for relative and absolute quantitation methods of quantitative proteomics were applied for analysis of the 53 proteins that were differentially expressed after treatment with juglone. Combined with verification experiments, such as detection of changes in DNA and RNA content and quantification of oxidative damage, our results suggested that juglone effectively increased the protein expression of oxidoreductase and created a peroxidative environment within the cell, significantly reducing cell wall formation and increasing membrane permeability. We hypothesize that juglone binds to DNA and reduces DNA transcription and replication directly. This is the first study to adopt a proteomic approach to investigate the antibacterial mechanism of juglone.

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We investigated the cytoprotective effects of anthocyanins in Aronia melanocarpa against apoptosis induced by Aβ1–42, a key mediator of AD pathophysiology. We measured intracellular calcium with a colorimetric kit, cellular apoptosis with DAPI, intracellular ROS with the fluorescent marker 2,3-dimethoxy-1,4-naphthoquinone, mitochondrial membrane potential with JC-1, and ATP with a colorimetric kit. Gene transcription and protein expression levels of calmodulin, cytochrome c, caspase-9, cleaved caspase-3, Bcl-2, and Bax were analyzed by RT-PCR and Western blotting. The results showed that pretreatment with anthocyanins significantly inhibited Aβ1–42-induced apoptosis, decreased intracellular calcium and ROS, and increased ATP and mitochondrial membrane potential. RT-PCR and Western blotting revealed that anthocyanins upregulated the gene transcription and protein expression of calmodulin and Bcl-2 and downregulated those of cytochrome c, caspase-9, cleaved caspase-3, and Bax. A. melanocarpa anthocyanins protected SH-SY5Y cells against Aβ1–42-induced apoptosis by regulating Ca2+ homeostasis and apoptosis-related genes and inhibiting mitochondrial dysfunction.

Aronia melanocarpa polyphenols (AMPs) can alleviate the degree of liver diseases in rats. However, the mechanism by which this is achieved through gut microbiota modulation remains unclear. Here, a rich-polyphenol extract of A. melanocarpa (AMPs) was used to treat lipopolysaccharide (LPS)-induced liver diseases in rats. To gain insights into the anti-LPS-induced liver disease, liver function index, expression of apoptosis proteins, inflammatory factors, and activation of inflammatory signaling pathways were determined with western blot analysis, immunohistochemistry, and 16S rRNA sequencing or quantitative real-time polymerase chain reaction (qRT-PCR). After AMPs treatment, the gut microbiota composition was modulated, promoting the intestinal barrier function by increasing the expression of intestinal epithelial cell tight junction proteins to reduce the LPS content in serum. The expression levels of inflammatory factors interleukin 6 (IL-6), interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), and related mRNAs were reduced. These results showed that AMPs, as a bioactive substance, could enhance the intestinal barrier function and modulate the gut microbiota of LPS-induced liver diseases.