Variety, geographical origin, and harvest season are important factors affecting the accumulation of polyphenols in Lycium barbarum. In this study, the effects of these factors on the polyphenolic components of this species were analyzed using ultra-performance liquid chromatography ion mobility quadrupole time-of-flight mass spectrometry. Moreover, the in vitro antioxidant activities of fruit extracts from this species were evaluated. The total polyphenolic contents of L. barbarum fruits from Jinghe County in Xinjiang and Zhongning County in Ningxia were 5.52–11.72 and 7.06–9.37 mg (gallic acid equivalent)/g dry weight, while the total flavonoid contents of L. barbarum fruits from these regions were 12.52–30.29 and 12.67–20.77 mg (rutin equivalent)/g dry weight, respectively. Overall, 39 types of polyphenols were identified in the fruit extracts, including 26 flavonoids, 10 phenolic acids, and three tannins. Of these, 11 polyphenols were quantitatively analyzed, which revealed rutin to be the most dominant polyphenolic component in fruits from Jinghe and Zhongning. There were significant differences (p < 0.05) in the polyphenolic contents and antioxidant activities of L. barbarum fruit extracts, depending on the geographical origin, variety, and harvest season. The antioxidant activity of this species was found to be significantly positively correlated with the polyphenolic contents. This study provided scientific guidance for comprehensive applications of polyphenols from different varieties of L. barbarum from separate geographical origins.

This study investigates pesticide levels in celery, and compares their degradation, dissipation, distribution, and dietary risk after spraying with selenium (Se) nanoparticles. Abamectin, imidacloprid, acetamiprid, thiamethoxam, and lambda-cyhalothrin were sprayed at 1.6, 6.8, 2.0, 1.0, and 0.7 g a.i. ha⁻¹ followed by a 2 g·ha⁻¹ Se nanoparticle application during the growing period. Thiamethoxam, abamectin, imidacloprid, lambda-cyhalothrin, and acetamiprid in celery degraded following a first order kinetic model after 2 g·ha⁻¹ Se nanoparticles application. With the exception of acetamiprid, the half-lives of thiamethoxam, abamectin, imidacloprid, and lambda-cyhalothrin were reduced from 2.4, 0.5, 1.2, 4.2 days without Se nanoparticles application to 1.4, 0.2, 0.9, 3.7 days with the addition of Se nanoparticles (2 g·ha⁻¹), respectively. The chronic dietary exposure risk probability (RQc) and the acute dietary exposure risk probability (RQa) of celery after Se nanoparticles application were within acceptable limits for consumption except for abamectin.

LBP (300 μg/mL) partially restores glucose consumption and glycogen content. Transcriptomic analysis suggests that these protective effects are potentially associated with the upregulation of glycerophospholipid–DAG-PtdOH signaling and ULK1-dependent autophagy. These preliminary findings provide transcriptional insights into a potential dual botanical mechanism, though further protein-level validation is required. Objective: The objective of this study was to investigate the ameliorative effects of LBP on palmitic acid (PA)-induced cellular dysfunction (or insulin signaling impairment) in HepG2 cells and the potential molecular mechanisms. Methods: LBP was extracted by hot water extraction–ethanol precipitation and characterized by the phenol-sulfuric acid method, Fourier-transform infrared spectroscopy (FT-IR) and nuclear magnetic resonance (NMR) spectroscopy for content determination and structural characterization. The CCK-8 assay was used to determine the safe concentrations of PA and LBP. Glucose consumption and glycogen content were measured by the glucose oxidase method. Transcriptome sequencing combined with GO and KEGG enrichment analyses was performed to screen key pathways and differentially expressed genes (DEGs). RT-qPCR was used to validate the mRNA expression of DGKA, LPIN1, and ULK1. Results: LBP was identified as a pyranose-type acidic heteropolysaccharide containing uronic acid. Compared with the control group, PA treatment significantly decreased glucose consumption and glycogen content (p < 0.05), both of which were significantly ameliorated by 300 μg/mL LBP intervention (p < 0.05). Transcriptome sequencing identified 1752 DEGs, and KEGG enrichment analysis indicated that LBP treatment was associated with transcriptional changes in glycerophospholipid metabolism, AMPK signaling, and autophagy pathways. RT-qPCR further showed that LBP significantly upregulated the mRNA expression of DGKA, LPIN1, and ULK1 (p < 0.05). However, these mechanistic insights are limited to the transcriptional level and require further protein-level validation. Conclusions: LBP exhibited protective effects against PA-induced insulin signaling impairment in HepG2 cells, which were potentially associated with the transcriptional regulation of the DAG-PtdOH metabolic axis and AMPK/ULK1 pathway-related genes. However, these mechanistic inferences are speculative and require validation via protein and inhibitor experiments.