Chitosan treatment reduces softening and chilling injury in cold-stored Hami melon by regulating starch and sucrose metabolism

Cold-stored Hami melon is susceptible to chilling injury, resulting in quality deterioration and reduced sales. Pre-storage treatment with chitosan reduces fruit softening and chilling injury in melon; however, the underlying mechanism remains unclear. In this study, Gold Queen Hami melons were treated with 1.5% chitosan solution for 10 min before cold storage at 3°C and then the effect of chitosan was examined on fruit firmness, weight loss, chilling injury, soluble solid content (SSC), pectin, and soluble sugar contents of melon fruit. Also, the enzyme activities and gene expressions related to fruit softening and starch and sucrose metabolism were investigated. Chitosan treatment reduced the fruit softening and chilling injury, maintained the high levels of starch and sucrose contents, and regulated the enzyme activities and gene expressions related to starch and sucrose metabolism. Fruit firmness was significantly positively correlated with sucrose and starch contents. Altogether, we uncovered the potential mechanism of chitosan coating mitigating melon softening and chilling injury through the regulation of starch and sucrose metabolism

Stability of the phenolic compounds and antioxidant capacity of five fruit (apple, orange, grape, pomelo and kiwi) juices during \u3ci\u3ein vitro\u3c/i\u3e-simulated gastrointestinal digestion

The in vitro digestive stability of phenolic compounds and the antioxidant capacity of five kinds of commonly consumed fruit juices in the daily diet, including apple juice (AJ), orange juice (OJ), grape juice (GJ), pomelo juice (PJ) and kiwifruit juice (KJ), were studied. Following in vitro digestion, the total phenolic (TP) content of fruit juices decreased to different extents by 35%, 25.3%, 23.5%, 22.2% and 7.8% for KJ, OJ, PJ, GJ and AJ, respectively. The individual phenolic content showed similar changes to the TP content, showing reductions of naringenin-trisaccharide in OJ and PJ, epicatechin in GJ, and chlorogenic acid in AJ by 43.74%, 27.59%, 47.11% and 33.28%, respectively. Conversely, the antioxidant capacity of fruit juices during digestion measured by ABTS assay increased from 4.79% to 35.53%, except in KJ, which decreased by 19.34%. These results show the health benefits of fruit juices after processing and contribute towards establishing suitable dietary recommendations

Stability of the phenolic compounds and antioxidant capacity of five fruit (apple, orange, grape, pomelo and kiwi) juices during \u3ci\u3ein vitro\u3c/i\u3e-simulated gastrointestinal digestion

The in vitro digestive stability of phenolic compounds and the antioxidant capacity of five kinds of commonly consumed fruit juices in the daily diet, including apple juice (AJ), orange juice (OJ), grape juice (GJ), pomelo juice (PJ) and kiwifruit juice (KJ), were studied. Following in vitro digestion, the total phenolic (TP) content of fruit juices decreased to different extents by 35%, 25.3%, 23.5%, 22.2% and 7.8% for KJ, OJ, PJ, GJ and AJ, respectively. The individual phenolic content showed similar changes to the TP content, showing reductions of naringenin-trisaccharide in OJ and PJ, epicatechin in GJ, and chlorogenic acid in AJ by 43.74%, 27.59%, 47.11% and 33.28%, respectively. Conversely, the antioxidant capacity of fruit juices during digestion measured by ABTS assay increased from 4.79% to 35.53%, except in KJ, which decreased by 19.34%. These results show the health benefits of fruit juices after processing and contribute towards establishing suitable dietary recommendations

Encapsulation Mechanism of Oxyresveratrol by β-Cyclodextrin and Hydroxypropyl-β-Cyclodextrin and Computational Analysis

In this study, the encapsulation mechanism of oxyresveratrol and β-cyclodextrin (β-CD) and hydroxypropyl-β-cyclodextrin (HP-β-CD) was studied. As this research shows, oxyresveratrol and two cyclodextrins (CDs) were able to form inclusion complexes in a 1:1 stoichiometry. However, the interaction with HP-β-CD was more efficient, showing up as higher encapsulation constant (KF) (35,864.72 ± 3415.89 M−1). The KF values exhibited a strong dependence on temperature and pH, which decreased as they increased. From the thermodynamic parameters (ΔH0, ΔS0, and ΔG0) of the oxyresveratrol loaded β-CD (oxyresveratrol-β-CD) and HP-β-CD (oxyresveratrol-HP-β-CD), it could be seen that the complexation process was spontaneous and exothermic, and the main driving forces between oxyrsveratrol and CDs were hydrogen bonding and van der waals force. Besides, molecular docking combined with 1H-NMR were used to explain the most possible mode of interactions between oxyresveratrol and CDs

High-Dose Vitamin C Tends to Kill Colorectal Cancer with High MALAT1 Expression

Background. Vitamin C (Vc) deficiency is frequently observed in cancer sites and has been proposed to have an antitumor effect. However, the mechanism of Vc’s killing effect is not clear. Besides, epigenetic alterations exhibit significant effects on colorectal cancer (CRC). This study aimed to explore the mechanism of Vc’s killing effect and its association to epigenetic alterations in CRC. Methods. Cell morphology, apoptosis, proliferation, and cycle were assayed to test Vc’s suppressive function in CRC cell lines. Xenograft and peritoneal implantation metastasis models were performed to evaluate the high-dose Vc’s inhibitory effect on tumor growth and metastasis. Immunohistochemistry was used to measure CD31 expression in solid tumors. A literature summary was applied for screening differently expressed long noncoding RNAs (lncRNAs) in CRC tissues and was closely associated with CRC progression. The qPCR was used to detect the expression of these lncRNAs. The association between Vc and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) was evaluated in MALAT1-transfected CRC cells and a xenograft model. Results. Vc was confirmed to function in proliferation suppression, apoptosis induction, and S phase arresting in CRC cell lines. High-dose Vc, but not physiologically low-dose Vc, was identified as a suppressive function on tumor growth in xenograft models and an inhibitory effect on implantation metastasis in peritoneal implantation metastasis mice. Furthermore, a consistent downregulation of MALAT1 induced by Vc was verified among CRC cell lines and tumor tissues from both mouse models. Finally, experiments on MALAT1-knockdown CRC cells and its xenograft model suggested that Vc had a tendency in killing CRC with high MALAT1 expression. Conclusions. Our findings demonstrate that high-dose Vc has more efficiency in suppressing CRC with higher MALAT1 expression. It gives high-dose Vc the possibility of a better curative effect on CRC with overexpressed MALAT1. Further clinical studies are still needed

The Severity of CVB3-Induced Myocarditis Can Be Improved by Blocking the Orchestration of NLRP3 and Th17 in Balb/c Mice

Background. The functional characteristics of NLRP3 in the pathogenesis of coxsackievirus B3- (CVB3-) induced viral myocarditis (VMC) have not been fully elucidated, and the targeted therapeutic effect of NLRP3 or its related pathway in VMC has not been reported. Method. In this work, the change patterns of NLRP3- and Th17-related factors were detected during the pathological process of CVB3-induced VMC in Balb/c mice. The correlation between NLRP3 and Th17 cells during the VMC process was analyzed by Spearman test. The coculture system of spleen CD4+ T and bone marrow CD11c+ DC cells was set to explore the orchestration of NLRP3 and Th17 in the pathological development of VMC in vitro. Anti-IL-1β antibody or NLRP3-/- Balb/c were used to block the NLRP3 pathway indirectly and directly to analyze the NLRP3-targeting therapeutic value. Results. The change patterns of NLRP3- and Th17-related molecules in the whole pathological process of mouse CVB3-induced VMC were described. Through Spearman correlation analysis, it was confirmed that there was a close correlation between NLRP3 and Th17 cells in the whole pathological process of VMC. And the interaction mode between NLRP3 and Th17 was preliminarily explored in the cell experiment in vitro. Under the intervention of an anti-IL-1β antibody or NLRP3 knockout, the survival rate of the intervention group was significantly improved, the degree of myocardial inflammation and fibrosis was significantly alleviated, and the content of myocardial IL-17 and spleen Th17 was also significantly decreased. Conclusion. Our findings demonstrated a key role of the NLRP3 inflammasome and its close relationship with Th17 in the pathological progression of CVB3-induced VMC and suggested a possible positive feedback-like mutual regulation mechanism between the NLRP3 inflammasome and Th17 in vitro and in the early stage of CVB3 infection. Taking NLRP3 as a new starting point, it provides a new target and idea for the prevention and treatment of CVB3-induced VMC