Feng Wang,Dongjie Liu,Ruijing Liu,Qin Wang,Gengsheng Xiao,Lukai Ma
Alternaria alternata is a common fruit-decaying fungus that is potentially hazardous to fruit quality and human health. In this study, volatile and non-volatile compounds in cherry quality after artificial inoculation with A. alternata during cold storage were investigated using HS-GC-IMS and LC-MS. After fungal exposure, cherry samples exhibited significant changes in fungal counts, fruit firmness, and total soluble solid. A total of 36 volatile compounds, including 15 alcohols, 9 aldehydes, 5 esters, 4 ketones, 2 sulfur compounds, and 1 hydrocarbon were detected in the cherries by HS-GC-IMS. Changes in various aldehydes and sulfur compounds occurred in the early and middle storage stages, and changes in alcohols, esters, and ketones occurred in the middle-later storage stages. Seven types of non-volatile compounds were identified as key differential metabolites including 2-hydroxyphenylacetic acid O-b-D-glucoside, 2-O-benzoyl-D-glucose, gluconic acid, D-glucuronic acid, malonic acid, portulacaxanthin II, and altenusin, which are involved in the biosynthesis pathways of glucose, glycoside compounds, betalain, and fungal metabolites. This study provides further understanding of the relationship between the contamination of A. alternata and the quality of cherry fruit and lays the foundation for preservation technology for fresh fruit.
This study aimed to determine the anti-obesity effects and mechanisms of Cerasus humilis polyphenol (CHP) in C57BL/6 obese mice and 3T3-L1 cells. High-performance liquid chromatography–electrospray ionization-tandem mass spectrometry was used for the qualitative and quantitative identification of CHP components. The obese mice, induced by feeding high-fat diet (HFD), were treated with CHP (250 mg/kg/day) by gavage for 12 weeks. Orlistat was gavaged at 15.6 mg/kg bw/day, as a positive control group. The analysis revealed that the main components of CHP were procyanidin B2, cyanidin-3-glucoside, and pelargonidin-3-glucoside. CHP dietary supplementation significantly reduced body weight and improved blood lipid measurements in HFD-fed mice (p < 0.01). Moreover, it inhibited mRNA expression of miR-122, Srebp-1c, and Cpt1a (p < 0.01) and reduced hepatic lipid deposition, as seen by hematoxylin and eosin staining. CHP downregulated the protein expression of PPARγ and C/EBPα in HFD-induced obese mice and inhibited adipocyte differentiation (p < 0.01). Compared with the HFD group, CHP supplementation had an obvious anti-inflammatory effect (decreased protein expression, such as TNF-α, IL-6, and MCP1), reducing leptin levels and TNF-α secretion in serum and cells (p < 0.01). CHP significantly inhibited the expression of miR-27a/b (53.3 and 29.9%, p < 0.01) in mice retroperitoneal white adipocytes, enhancing the expression of the target gene Prdm16 and significantly upregulating Sirt1 (105.5%, p < 0.01) compared with the HFD group. Moreover, CHP supplementation effectively improved oxidative stress (ROS, T-AOC, SOD, CAT, and GSH-Px) induced by HFD in obese mice (p < 0.01). Thus, CHP mitigates adipocyte differentiation, browning of white adipocytes, and reduction of inflammation and antioxidant activity to reduce obesity. Consequently, these results provide novel insights into the anti-obesity roles of CHP in HFD-induced obesity.
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