Effect and Mode of Different Concentrations of Citrus Peel Extract Treatment on Browning of Fresh-Cut Sweetpotato.

Browning is one of the main phenomena limiting the production of fresh-cut sweetpotatoes. This study investigated the anti-browning effect of citrus peel extracts and the key components and modes of action associated with browning in fresh-cut sweetpotatoes. Five different concentrations of citrus peel extract (1, 1.5, 2, 2.5 and 3 g/L) were selected to ensure storage quality; and the physical and chemical properties of fresh-cut sweetpotato slices were analysed. A concentration of 2 g/L of citrus peel extract significantly inhibited the browning of fresh-cut sweetpotatoes. The results showed that the browning index and textural characteristics of fresh-cut sweetpotatoes improved significantly after treatment with citrus peel extract; all the citrus peel extract solutions inhibited browning to some extent compared to the control. In addition; LC-IMS-QTOFMS analysis revealed a total of 1366 components in citrus peel extract; the evaluation of citrus peel extract monomeric components that prevent browning in fresh-cut sweetpotato indicated that the components with better anti-browning effects were citrulloside, hesperidin, sage secondary glycosides, isorhamnetin and quercetin. The molecular docking results suggest that citrullosides play a key role in the browning of fresh-cut sweetpotatoes. In this study, the optimum amount of citrus peel extract concentration was found to be 2 g/L.

Baicalin Ameliorates Lung Injury in Rats by Inhibiting NLRP3 Inflammasome Activation via NF-[Formula: see text]B Signaling Pathway.

Hemorrhagic shock (HS) is defined as a reduction in tissue oxygenation and organ dysfunction due to severe blood loss. Lung injury is a frequent complication of HS. Baicalin, isolated from Radix Scutellariae, has been reported to profile the antitumor, anti-oxidative, anti-inflammatory, and antibacterial roles in various pathological processes. Nevertheless, the effects of baicalin on HS-induced lung injury are unclear. This study aims to examine the therapeutic effects of baicalin on lung injury. We first established the lung injury rat models by withdrawing blood in the femoral artery followed by resuscitation. A pathological analysis showed that HS-administrated rats presented severe capillary leakage and pulmonary edema, while baicalin therapy alleviated the symptoms. Baicalin therapy reduced the number of macrophages and neutrophils in bronchoalveolar lavage fluid and decreased the expression and activity of myeloperoxidase (neutrophile infiltration marker) in the lung tissues of HS rats, indicating that baicalin alleviated HS-induced infiltration of inflammatory cells. The secretion of inflammatory cytokines, including interleukin (IL)-1[Formula: see text], IL-6, IL-18, and tumor necrosis factor [Formula: see text] (TNF-[Formula: see text]), as well as the activation of the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing-3 (NLRP3) inflammasome, were inhibited by baicalin administration. Furthermore, we found that the NF-[Formula: see text]B pathway, a canonical pro-inflammatory pathway, was also blocked after treatment with baicalin in HS-evoked rats, as indicated by the decreased expression of p65 and p65 phosphorylation in the lung tissues. In summary, we infer that baicalin may exert a protective role in HS-induced lung injury by suppressing the activation of NLRP3 inflammasome via the NF-[Formula: see text]B pathway.

Involvement of NADPH oxidase in patulin-induced oxidative damage and cytotoxicity in HEK293 cells.

Patulin (PAT) is a kind of mycotoxins that commonly found in decayed fruits and their products. Our previous studies have shown that PAT induced cell apoptosis and the overproduction of reactive oxygen species (ROS) in human embryonic kidney (HEK293) cells. The present study aimed to further investigate the functional role of NADPH oxidase, one of the main cellular sources of ROS, in PAT-induced apoptosis and oxidative damage in HEK293 cells. We demonstrated that the protein and mRNA expression levels of NADPH oxidase catalytic subunit NOX2 and regulatory subunit p47phox were up-regulated under PAT stress. Inhibiting of NADPH oxidase with the specific antagonist diphenyleneiodonium (DPI) suppressed cytotoxicity and apoptosis induced by PAT as evidenced by the increase of cell viability, the decrease of LDH release and the inhibition of caspase activities. Furthermore, DPI re-established mitochondrial membrane potential (MMP) and enhanced cellular ATP content. Importantly, DPI supplementation elevated endogenous GSH contents as well as the ratio of GSH/GSSG. Meanwhile, the antioxidant-enzyme activities of GPx, GR, CAT and SOD were significantly promoted. Collectively, our results suggested that NADPH oxidase played a critical role in PAT-induced nephrotoxicity, and inhibition of NADPH oxidase by DPI attenuated cell injury and apoptosis via regulation of oxidative damage.