Cellulose (C) and Antarctic krill protein (AKP) were dissolved at low temperature, and then C/AKP composite fibers were prepared by wet spinning. In this paper, the effect of coagulation bath temperature on the properties of C/AKP composite fibers were studied by FT-IR, XRD, DSC, and other tests. The results showed that, when the temperature of the coagulation bath increased from 5 to 25 °C, the intermolecular hydrogen bond content of the C/AKP composite fibers increased from 28.20% to 31.33%. When the coagulation bath temperature is 15 °C, the breaking strength of the composite fibers is 1.64cN/ dtex, which is 12% higher than that of the composite fibers at room temperature. At this temperature, the crystallinity of the composite fibers is improved, the thermal stability is slightly improved, and the surface morphology is smoother. Inspiringly, when zinc sulfate is added to the coagulation bath, the formation process of the fibers is milder. Moreover, the C/AKP composite fibers have excellent antibacterial activity against Escherichia coli and Staphylococcus aureus.

Background: Gallic acid (GA) is a natural small-molecule polyphenol having a wide range of pharmacological activities. Until now, some works have studied the effect and the mechanisms of GA against inflammation. However, whether or how gallic acid regulates the downstream metabolic disorder against acute inflammation remains unclear. The present study explored the protective effect and the potential mechanism of GA on acute inflammation through the metabolomics approach.Methods: An acute inflammation rat model was induced by local injection of carrageenin. Local swelling on paw and serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) were assessed in Control, Model and Gallic acid groups, respectively. Serum metabolomics based on high-performance liquid chromatography coupled with mass spectrometry (HPLC-MS) was also established to collect rats’ metabolic profiles and explore the metabolic changes related to GA pretreatment.Results: Compared to the Modal group, local pain, redness, and swelling induced by carrageenin were significantly alleviated in GA groups in addition to the dose-dependent decreases of TNF-α and IL-6. Metabolomics analysis found significant alterations in metabolic signatures between the carrageenin-induced inflammation and control groups. Twelve potential biomarkers were further identified in acute inflammation by principal component analysis (PCA) and partial least squares discrimination analysis (PLS-DA). In addition, when rats were pretreated with gallic acid, serum levels of eleven biomarkers were observed to restore partially. Metabolic pathway and networks analysis revealed that GA might invert the pathological process of acute inflammation by regulating the key biomarkers involved in linoleic acid metabolism, ascorbate and aldarate metabolism, pentose and glucuronate interconversions, and arachidonic acid (AA) metabolism pathways.Conclusion: The study elucidates the protective effect of gallic acid against acute inflammation and its possible regulating mechanism from a metabolomic perspective. These results could provide a theoretical basis for clarifying gallic acid’s mechanism and potential medicinal value in curing inflammation disorder in the clinic.

Background: Hepatocellular carcinoma (HCC), as an aggressive cancer with a high mortality rate, needs high-efficiency and low-toxicity drug therapy. Natural products have great potential as candidate lead compounds for the development of new HCC drugs. Crebanine is an isoquinoline alkaloid derived from Stephania with various potential pharmacological effects such as anti-cancer. However, the molecular mechanism underlying crebanine-induced liver cancer cells apoptosis has not been reported. Here, we investigated the effect of crebanine on HCC and identified a potential mechanism of action.Methods: In this paper, we intend to detect the toxic effects of crebanine on hepatocellular carcinoma HepG2 cells through a series of in vitro experiments, including detecting the effects of crebanine on the proliferation of HepG2 cells using the CCK8 method and plate cloning assay, observing the growth status and morphological changes of crebanine on HepG2 cells by inverted microscopy; and using the Transwell method to determine the the effect of crebanine on the migration and invasion ability of HepG2 cells; using Hoechst 33258 assay to stain cancer cells, thus observing the effect of crebanine on the morphology of HepG2 apoptotic cells, and detecting the apoptotic state and level of HepG2 cells by flow cytometry; using ROS kit and JC-1 assay kit to detect the changes of reactive oxygen species and mitochondrial membrane potential of HepG2 The immunofluorescence assay was taken to verify whether crebanine had an effect on the expression of p-FoxO3a in cancer cells; the Wetern blot assay was also used to examine the effect of crebanine on proteins related to the mitochondrial apoptotic pathway and its effect on the regulation of the relative protein expression of AKT/FoxO3a axis; after this, NAC and AKT inhibitor LY294002 were used to cells were pretreated with NAC and AKT inhibitor LY294002, respectively, in order to further validate the inhibitory effect of crebanine.Results: It was shown that crebanine effectively inhibited the growth and capacity of HepG2 cells migration and invasion in a dose-dependent manner. Furthermore, the effect of crebanine on the morphology of HepG2 cells was observed through microscopy. Meanwhile, crebanine induced apoptosis by causing reactive oxygen species (ROS) burst and mitochondrial membrane potential (MMP) disrupt. We found that crebanine could down-regulate Bcl-2 and up-regulate Bax, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9, but these effects were overturned by ROS inhibitor N-acetylcysteine (NAC). Crebanine also down-regulated p-AKT and p-FoxO3a, and the PI3K inhibitor LY294002 significantly enhances this effect. We also found that the expression of AKT/FoxO3a signaling pathway was ROS-dependent. As shown by Western blots, NAC could partially attenuate the inhibitory effect of crebanine on AKT and FoxO3a phosphorylation.Conclusion: Based on our results, our results suggest that crebanine, as a compound with potential anticancer activity, has significant cytotoxic effects on hepatocellular carcinoma,and it likely induces apoptosis via ROS in the mitochondrial pathway and simultaneously affects the biological function of HCC via the ROS-AKT-FoxO3a signaling axis.

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Uridine is a key metabolite used as a substrate for the production of DNA, RNA, and glucose, and it is mainly synthesized in the liver. Currently, it is not known whether uridine levels are altered in the tumor microenvironment of patients with hepatocellular carcinoma (HCC) and whether uridine can be a target for tumor therapy. In this study, the detection of genes associated with de novo uridine synthesis, carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, dihydroorotase (CAD) (n = 115), and dihydroorotate dehydrogenase (DHODH) (n = 115) in HCC tissues through tissue microarrays revealed that the expression of CAD and DHODH was higher in tumor compared with paraneoplastic tissues. Next, we collected tumor tissues from surgically resected HCC patients and the corresponding adjacent non-tumor tissues (n = 46) for LC–MS/MS assays. The results showed that the median and interquartile ranges of uridine content in non-tumor and tumor tissues were 640.36 (504.45–807.43) and 484.22 (311.91–626.73) nmol/g, respectively. These results suggest that uridine metabolism is disturbed in HCC patients. To further investigate whether uridine can be used as a tumor-therapeutic target, a series of high concentrations of uridine were incubated with HCC cells in vitro and in vivo. It was observed that uridine dose-dependently inhibited the proliferation, invasion, and migration of HCC cells by activating the ferroptosis pathway. Overall, these results reveal for the first time the range of uridine content in human HCC tissues and suggest that uridine may be a new target for HCC therapy.