Diabetic nephropathy (DN) is a leading cause of end-stage renal disease, and the advanced glycation end products (AGEs) and their receptor RAGE play a critical pathogenic role in DN progression. This study investigated the therapeutic mechanisms of licochalcone A (LCA), a bioactive flavonoid from licorice, against DN with emphasis on AGEs/RAGE signaling modulation. Male C57BL/6J mice were used to establish a high-fat diet/streptozotocin-induced DN model, followed by 4-week treatment with LCA (5, 10, 20 mg/kg/day) or metformin (250 mg/kg/day). LCA treatment significantly improved glucose tolerance, reduced fasting blood glucose levels, and ameliorated characteristic renal pathological changes including mesangial matrix expansion and collagen deposition. Mechanistically, LCA suppressed AGEs accumulation in both serum and renal tissues while downregulating RAGE expression, thereby attenuating NF-κB-mediated inflammatory responses (TNF-α, IL-1β, IL-6). Furthermore, LCA mitigated oxidative stress by restoring SOD activity and reducing MDA and ROS levels, and alleviated endoplasmic reticulum stress through suppression of the GRP78/PERK/ATF4/CHOP pathway, consequently reducing renal cell apoptosis. Serum metabolomics revealed that LCA corrected lipid metabolism disorders, with KEGG enrichment analysis highlighting ABC transporter pathway involvement. LCA treatment reversed diabetic dyslipidemia, prevented ectopic lipid accumulation in kidneys, and modulated the SREBP-1c/ABCA1 axis. These findings were validated in high glucose-treated HK-2 cells. In conclusion, LCA demonstrates multi-targeted nephroprotective effects in DN through suppression of AGEs/RAGE signaling and downstream modulation of inflammation, oxidative stress, endoplasmic reticulum stress, and lipid metabolism dysregulation.

Reactive carbonyl species (RCS) represent a diverse class of electrophilic compounds ubiquitously present in environmental, dietary, and biological systems, posing significant challenges for human health risk assessment. This review systematically examines the classification, formation mechanisms, toxicological profiles, and health risk assessment frameworks for RCS, with particular emphasis on food-derived compounds. RCS are classified into three major categories: monocarbonyl compounds, polycarbonyl compounds, and α,β-unsaturated carbonyls. Each category exhibits distinct reactivity patterns and biological effects. These compounds are generated through both exogenous pathways, primarily during food processing, and endogenous metabolic processes, including lipid peroxidation, amino acid oxidation, and glycation reactions. RCS exert toxicity through multiple molecular mechanisms. These include protein carbonylation, DNA adduct formation, advanced glycation end product (AGE) generation, and disruption of cellular signaling pathways. Such molecular events contribute to the pathogenesis of diabetes, cardiovascular disease, neurodegeneration, and cancer. Human metabolism of RCS involves Phase I reactions catalyzed by aldehyde dehydrogenases and aldo-keto reductases, followed by Phase II conjugation via glutathione S-transferases. Genetic polymorphisms in these metabolic enzymes create substantial inter-individual variations in RCS susceptibility. Contemporary risk assessment approaches integrate classical food safety frameworks with mechanistic toxicology principles. Current methodologies employ benchmark dose modeling, cumulative exposure assessment, and biomarker-guided evaluation strategies. Future advancement of RCS risk assessment requires development of integrated assessment models, validation of exposure and effect biomarkers, application of physiologically-based pharmacokinetic (PBPK) modeling, and international regulatory harmonization through sustained interdisciplinary collaboration.

Essential oils (EOs), complex mixtures of volatile organic compounds derived from aromatic plants, have demonstrated significant therapeutic potential for neurological and psychiatric disorders through multi-targeted mechanisms. This comprehensive review synthesizes current evidence regarding the neurological effects of essential oil components, with emphasis on psychiatric disorders (depression and anxiety), sleep disorders (insomnia), and neurodegenerative diseases (particularly Alzheimer’s disease). The major bioactive constituents—including monoterpenes (linalool, α-pinene, limonene, 1,8-cineole), sesquiterpenes (β-caryophyllene, patchoulol), and phenylpropanoids (cinnamaldehyde, eugenol)—exert neuroprotective effects through convergent mechanisms despite compositional diversity. These mechanisms encompass modulation of neurotransmitter systems (GABAergic, serotonergic, dopaminergic, cholinergic), regulation of the hypothalamic-pituitary-adrenal axis, anti-inflammatory and antioxidant activities, inhibition of pathological protein aggregation, enhancement of neurotrophic factor expression, and receptor-mediated neuroprotection involving GABAA and cannabinoid type 2 (CB2) receptors. The convergence of diverse phytochemical compositions on common therapeutic targets suggests potential for personalized approaches based on individual tolerability profiles, while the multi-targeted nature of EOs aligns with the multifactorial pathogenesis of neurological disorders, supporting their investigation as complementary therapeutic strategies.

Selenoflavonoids (SeFs), emerging as a novel class of bioactive compounds that integrate selenium into flavonoid structures, have garnered significant attention due to their enhanced biological properties compared to conventional flavonoids. This review systematically analyzes recent advances in SeFs research, encompassing their structural characteristics, metabolic processes, and diverse biological functions. Studies reveal that selenium incorporation occurs primarily through the formation of covalent bonds between phenolic hydroxyl groups and selenium in its +4 oxidation state, resulting in compounds with superior bioavailability and reduced toxicity compared to inorganic selenium forms. The metabolic fate of SeFs involves complex pathways centered on hydrogen selenide (H2Se) as a crucial intermediate, with subsequent transformations regulated by selenium status and metabolic requirements. Extensive investigations demonstrate that SeFs exhibit remarkable therapeutic potential across multiple biological systems, including enhanced anti-inflammatory and antioxidant activities through NF-κβ pathway modulation and GPx-mimetic properties, neuroprotective effects via regulation of protein aggregation and neuroinflammation, metabolic benefits through modulation of glucose and lipid homeostasis, and antitumor activities targeting multiple cellular pathways. Current challenges in SeFs research include the optimization of isolation techniques, scalable synthesis methodologies, and the need for deeper mechanistic understanding of their biological activities. These findings suggest that SeFs represent promising candidates for therapeutic applications, though further research is needed to fully elucidate their molecular mechanisms and clinical potential.

(+)-Catechin (CE) is mainly found in green and black tea and has many biological effects, such as anti-inflammatory, anti-cancer, anti-viral effects, protecting human organs, especially the kidney. This study aims to identify the circRNAs induced by CE in db/db mice and their roles in diabetic nephropathy progression. After the db/db mice were treated with CE, RNA-seq was performed to identify the differentially expressed circRNA and mRNAs. The ceRNA regulatory network was constructed and analyzed using bioinformatics software and public databases (Cytoscape, ClueGO, MiRWalk, STRING, et al.). Our results revealed that 6 differentially expressed circRNAs are most associated with the cholinergic synapse, neurotrophin signaling pathway, and insulin signaling pathway. Among these, circRNA.5549 and circRNA.4712 might regulate Cd36, Cyp26b1, C8a, Cyp2j13, Grem2 genes through ceRNA regulatory mechanism in the presence of CE treatment. The expanded network of proteins interacting with these 5 genes shows that the TGF-β signaling pathway, signaling pathways regulating pluripotency of stem cell, fat digestion and absorption, and PPAR signaling pathway was highly enriched. Overall, circRNA.5549 and circRNA.4712 exhibit a promotive function in CE-treated db/db mice, especially in circRNA.5549/miR-29a-5P/Cd36 regulatory network, and this evidence suggest that their ceRNA regulatory network might be a therapeutic target for DN in humans.

This study established a method for the simultaneous determination of 74 pesticide residues in Panax notoginseng by QuEChERS pretreatment method coupled with GC-MS/MS, and carried out pesticide residue analysis on 20 batches of market samples in China. The samples were extracted with acetonitrile, cleaned up with primary secondary amine (PSA) and octadecylsilane (C₁₈) and determined by GC-MS/MS in multiple reaction monitoring (MRM) mode. Matrix-matched calibration was recommended to combat the matrix effect. A good linearity was observed in the range of 10−500 ng/mL with correlation coefficients ≥ 0.9950. The mean recoveries for most of the pesticides were in the range of 70%−120% with RSD < 20%. The limits of detection ranged 0.28–2.00 μg/kg, while the limits of quantification were 0.94–6.65 μg/kg. Following the application of "top-down" approach, the expanded measurement uncertainty for all the analytes was < 30%. The proposed method was successfully applied to determine pesticide residues in 20 market samples in China, where 9 pesticides were detected and quintozene exceeded the criteria domestically and abroad.