Hua Wang

Naringin is one of the common flavonoids in grapefruit, which has anti-cancer, antioxidant, and anti-inflammatory activities. However, its poor solubility limits its wide application. Therefore, the aim of this study is to investigate the anti-inflammatory effect of naringin combined with chitooligosaccharides with good biocompatibility by constructing a mouse model of systemic inflammatory response syndrome (SIRS). The results showed that the naringin–chitooligosaccharide (NG-COS) complex significantly inhibited lipopolysaccharide (LPS)-induced weight loss, reduced food intake, tissue inflammatory infiltration, and proinflammatory cytokines IL-6, TNF-α, INF-γ, and IL-1β levels. The complex also significantly affected the content of malondialdehyde and the activities of MPO, SOD, and GSH in the liver, spleen, lungs, and serum of mice with systemic inflammation. In addition, NG-COS significantly inhibited the mRNA expression of inflammatory factors in the TLR4/NF-κB signaling pathway. Principal component analysis showed that the complexes could inhibit LPS-induced systemic inflammation in mice, and the effect was significantly better than that of naringin and chitooligosaccharides alone. This study explored the synergistic effects of chitosan and naringin in reducing inflammation and could contribute to the development of novel biomedical interventions.

Light-induced off-flavor compounds in Ponkan mandarin juice were investigated during its shelf-life by headspace solid-phase microextraction multidimensional gas chromatography–mass spectrometry/olfactometry (MDGC-MS/O) and a GC–MS/pulsed flame photometric detector (GC–MS/PFPD). A total of 34 aroma-active compounds with flavor dilution (FD) factors from 2 to 128 were tentatively identified by aroma extract dilution analysis-MDGC-MS/O. Among them, a light-induced off-flavor compound with a high FD factor, methional (cooked potato), was positively identified in the Ponkan mandarin juice at the end of the shelf-life. In addition, 11 volatile sulfur compounds (VSCs), including 6 screened shelf-markers (variable identification, VID > 0.80), were identified in Ponkan mandarin juice by a sulfur detector (PFPD). Four VSCs exhibited odor activity values exceeding 1. Three VSCs (methanethiol, dimethyl trisulfide, and methional) were confirmed as key light-induced off-flavor compounds in Ponkan mandarin juice based on addition/omission experiments. Furthermore, light irradiation accelerated the degradation of sulfur precursors (methionine and MMS) and the formation of these VSCs leading to an increase in off-flavor intensity.

An efficient and practical method for identifying mandarin juice over-blended into not from concentrate (NFC) orange juice was established. Juices were extracted from different cultivars of sweet orange and mandarin fruits. After being pasteurized, the volatile organic compounds (VOCs) in the juice samples were extracted using headspace solid-phase microextraction, and qualitatively and quantitatively analyzed using gas chromatography–mass spectrometry detection. Thirty-two VOCs contained in both the sweet orange juice and mandarin juice were used as variables, and the identification model for discriminating between the two varieties of juice was established by principal component analysis. Validation was applied by using common mandarin juices from Ponkan, Satsuma and Nanfengmiju cultivars blended at series of proportions into orange juices from Long-leaf, Olinda, and Hamlin cultivars. The model can visually identify a blending of mandarin juice at the volume fraction of 10% or above.

The prophylactic effects of the polymethoxyflavones (PMFs) in long-leaf orange peel oil (OPO) were determined using an N^ω-nitro-L-arginine-induced hypertensive rat model. The OPO contained eight PMF components, namely sinensetin, hexamethoxyflavone, tetramethyl-O-isoscutellarein, nobiletin, tetramethyl-O-scutellarein, heptamethoxyflavone, 5-demethylnobiletin and tangeretin. After treatment with OPO, the SP (systolic pressure) and DP (diastolic pressure) in hypertensive rats were reduced. The NO (nitric oxide) contents in serum, heart, liver and kidney of OPO-treated N^ω-nitro-L-arginine (L-NNA)-induced hypertensive rats were higher than those in untreated hypertensive rats, but the MDA (malondialdehyde) contents in OPO-treated rats were lower than those of the control rats (untreated hypertensive rats). ET-1 (endothelin-1), VEGF (vascular endothelial growth factor) and E-selectin serum levels in hypertensive rats could be reduced, but the CGRP (calcium gene-related peptide) level could be increased by OPO treatment. The results of the qPCR assay showed that OPO upregulated HO-1 (heme oxygenase-1), nNOS (neuronal nitric oxide synthase) and eNOS (endothelial nitric oxide synthase) mRNA expression and downregulated ADM (adrenomedullin), RAMP2 (receptor activity modifying protein 2) and iNOS (inducible nitric oxide synthase) expression in hypertensive rats. The Western blot results also proved that OPO upregulated nNOS and eNOS protein expression and downregulated iNOS expression in hypertensive rats. Based on this study, we could conclude that OPO showed good antihypertensive effects, and the effect was concentration dependent.