Ginseng residue polysaccharides (GRP) at three levels were excellently blended into chitosan to form antioxidant composite films, which exhibited higher density, opacity and moisture, as well as lower water vapor permeability, tensile strength and elongation ratio than those of neat chitosan film. Thermogravimetry evidenced no difference in stability, and SEM and AFM revealed smooth and dense surfaces with no cracks and micropores, whereas structural analyses disclosed slight changes in films’ structures after adding GRP. A chitosan film containing 0.5% GRP (Chitosan + GRP) was then employed for a fruit preservation study. Fresh-cut melon covered with Chitosan + GRP displayed delayed deteriorating compared with other groups. A possible antioxidant mechanism in fruit preservation was then suggested, and PCA and correlation analyses supported these findings. The results demonstrated that our antioxidant chitosan films incorporated with GRP are quite promising for enabling the food industry to produce eco-friendly and sustainable packaging.

The study aimed, by integrating transcriptomics and metabolomics, to reveal novel biomarkers caused by overdosed acetaminophen (APAP) and liver protection substances procured by pre-administration of ginseng shoots extract (GSE). Totally 4918 genes and 127 metabolites were identified as differentially expressed genes and differential metabolites, respectively. According to KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment, such pathways as primary bile acid biosynthesis, bile secretion, retinol metabolism, histidine and several other amino-related metabolism were significantly altered by GSE and disturbed by subsequent overdosed APAP at the transcriptomic as well as metabolomic levels. Fifteen key biomarker metabolites related to these pathways were up-regulated in APAP-treated vs GSE-pretreated liver tissues, and were reported exerting anti-oxidant, anti-inflammatory, anti-apoptotic and/or immunomodulate functions, three of which even possessed direct hepatoprotection effects. Twenty five vital unigenes modulating these metabolites were further verified by correlation analysis and expression levels of fifteen of them were examined by qRT-PCR. Our findings indicate that GSE may be an effective dietary supplement for preventing the liver damage caused by the overdosed APAP.

Background/Objectives: Metabolic dysfunction-associated steatohepatitis (MASH) has become the leading cause of hepatocellular carcinoma and liver disorders globally. Nevertheless, only one expensive drug, resmetirom (Res), has been approved by the FDA for MASH treatment to date. However, its high price has imposed a heavy financial burden on patients. Methods: In this study, half-dose Res and low-dose metformin (Met) (referred to as RM) were administered in combination to treat MASH models in vitro and in vivo. We utilized transcriptome and lipidomics sequencing to assess the efficacy of RM in improving MASH. Our goal was to systemically compare the therapeutic effects of RM, Met, and Res on MASH and elucidate the underlying mechanisms. Results: Our results demonstrated that RM was comparable to Res and superior to Met in reducing lipid production in vitro, attenuating lipid accumulation, inhibiting inflammation, and improving fibrosis in vivo. Transcriptome and lipidome analyses further revealed that RM regulated the expression of genes and lipids in a manner similar to Res, particularly in pathways related to cholesterol metabolism and inflammation. Further validation showed that RM facilitated cholesterol transformation by robustly promoting the expression of CYP7A1, thereby mitigating MASH. Conclusions: Collectively, our findings highlight that a combination of half-dose Res and Met is equivalent to Res alone in terms of MASH treatment efficacy. This study provides a novel therapeutic strategy that is not only effective for MASH treatment but also reduces the economic burden on patients.