SOX9 promotes stemness in the CAL27 cell line of tongue squamous cell carcinoma.

Tongue squamous cell carcinoma (TSCC) is a prevalent form of oral malignancy, with increasing incidence. Unfortunately, the 5-year survival rate for patients has not exceeded 50%. Studies have shown that sex-determining region Y box 9 (SOX9) correlates with malignancy and tumor stemness in a variety of tumors. To investigate the role of SOX9 in TSCC stemness, we analyzed its influence on various aspects of tumor biology, including cell proliferation, migration, invasion, sphere and clone formation, and drug resistance in TSCC. Our data suggest a close association between SOX9 expression and both the stemness phenotype and drug resistance in TSCC. Immunohistochemical experiments revealed a progressive increase of SOX9 expression in normal oral mucosa, paracancerous tissues, and tongue squamous carcinoma tissues. Furthermore, the expression of SOX9 was closely linked to the TNM stage, but not to lymph node metastasis or tumor diameter. SOX9 is a crucial gene in TSCC responsible for promoting the stemness function of cancer stem cells. Developing drugs that target SOX9 is extremely important in clinical settings.

Identification of OLA1 as a Novel Protein Target of Vitexin to Ameliorate Dextran Sulfate Sodium-Induced Colitis with Tissue Thermal Proteome Profiling.

Vitexin, which exists in various medicinal plants and food sources, has recently received increasing attention because of its anti-inflammatory properties. This study aims to identify the protein target of vitexin that ameliorates dextran sulfate sodium (DSS)-induced colitis. The results showed that vitexin not only alleviated the clinical symptoms and colonic damage in mice with DSS-induced colitis but also suppressed the colonic production of inflammatory cytokines (IL-1ß, IL-6, ICAM, and VCAM) and enhanced the expression of barrier-associated proteins (ZO-1, Occludin, and E-cadherin). Based on tissue thermal proteome profiling (Tissue-TPP) and molecular docking, OLA1 was creatively identified as a potential protein target for vitexin. Further siRNA-mediated knockdown of the OLA1 gene in Caco-2 cells demonstrated the ability of OLA1 to increase Nrf2 protein expression and, thus, mediated the anti-inflammatory effects of vitexin. Interaction of the OLA1-vitexin complex with Keap1 protein to disrupt the Keap1-Nrf2 interaction may be required for activating Nrf2. Our findings revealed a novel role for OLA1 as a protein target of vitexin that contributes to its anti-inflammatory action by activating Nrf2, which may provide a promising molecular mechanism for novel therapeutic strategies to treat colitis and the associated systemic inflammation.

Ly6D facilitates chemoresistance in laryngeal squamous cell carcinoma through miR-509/ß-catenin signaling pathway.

Chemotherapy resistance is a major limiting factor in the cure of patients with laryngeal squamous cell carcinoma (LSCC). Lymphocyte antigen 6 superfamily member D (Ly6D) is highly expressed in various tumors, but its role and underlying molecular mechanisms in chemoresistance of LSCC cells remains largely unclear. In this study, we reveal that overexpression of Ly6D facilitates LSCC cell chemoresistance, while Ly6D silencing abolishes this phenotype. Moreover, bioinformatics analysis, PCR array, and functional analysis confirmed that activation of the Wnt/ß-catenin pathway contributes to Ly6D-mediated chemoresistance. The genetic and pharmacological inhibition of ß-catenin compromises chemoresistance mediated by Ly6D overexpression. Mechanistically, Ly6D overexpression significantly attenuates the expression of miR-509-5p, thereby unleashing its target gene CTNNB1 to activate Wnt/ß-catenin pathway and ultimately promote chemoresistance. In contrast, Ly6D augmenting ß-catenin-mediated chemoresistance in LSCC cells were reversed by ectopic expression of miR-509-5p. Furthermore, ectopic expression of miR-509-5p markedly repressed the two other targets, MDM2 and FOXM1. Taken together, these data not only reveal the key role of Ly6D/miR-509-5p/ß-catenin in chemotherapy resistance, but also provide a new strategy for the clinical treatment of refractory LSCC.

Pain management in patients with hepatocellular carcinoma after transcatheter arterial chemoembolisation: A retrospective study.

BACKGROUND: Pain after transcatheter arterial chemoembolisation (TACE) can seriously affect the prognosis of patients and the insertion of additional medical resources. AIM: To develop an early warning model for predicting pain after TACE to enable the implementation of preventive analgesic measures. METHODS: We retrospectively collected the clinical data of 857 patients (from January 2016 to January 2020) and prospectively enrolled 368 patients (from February 2020 to October 2022; as verification cohort) with hepatocellular carcinoma (HCC) who received TACE in the Hepatic Surgery Center of Tongji Hospital. Five predictive models were established using machine learning algorithms, namely, random forest model (RFM), support vector machine model, artificial neural network model, naive Bayes model and decision tree model. The efficacy of these models in predicting postoperative pain was evaluated through receiver operating characteristic curve analysis, decision curve analysis and clinical impact curve analysis. RESULTS: A total of 24 candidate variables were included in the predictive models using the iterative algorithms. Age, preoperative pain, number of embolised tumours, distance from the liver capsule, dosage of iodised oil and preoperative prothrombin activity were closely associated with postoperative pain. The accuracy of the predictive model was compared between the training [area under the curve (AUC) = 0.798; 95% confidence interval (CI): 0.745-0.851] and verification (AUC = 0.871; 95%CI: 0.818-0.924) cohorts, with RFM having the best predictive efficiency (training cohort: AUC = 0.869, 95%CI: 0.816-0.922; internal verification cohort: AUC = 0.871; 95%CI: 0.818-0.924). CONCLUSION: The five predictive models based on advanced machine learning algorithms, especially RFM, can accurately predict the risk of pain after TACE in patients with HCC. RFM can be used to assess the risk of pain for facilitating preventive treatment and improving the prognosis.

MYC-activated LINC00607 promotes hepatocellular carcinoma progression by regulating the miR-584-3p/ROCK1 axis.

BACKGROUND: There have been many reports of long non-coding RNAs (lncRNAs) in tumors, and abnormally expressed lncRNA is closely related to hepatocellular carcinoma (HCC). The mechanism of LINC00607 in HCC has not been reported. METHODS: We utilized qPCR to evaluate the RNA expression level. The mechanism of MYC binding to the LINC00607 promoter was revealed through chromatin immunoprecipitation assay and dual luciferase reporter assay. The proliferation and invasive ability were evaluated by CCK-8 and transwell assays. The relation between LINC00607 and miR-584-3p was assessed by RNA immunoprecipitation assay and dual luciferase reporter assay. The level of ROCK1 was evaluated by qPCR and western blot. RESULTS: In this research, we found that the expression of LINC00607 was higher in HCC tissues when compared with that in the adjacent non-tumor tissues. Meanwhile, MYC was observed to interact with the LINC00607 promoter, leading to the upregulation of LINC00607 in HCC. We further revealed that LINC00607 functioned as a sponge for miR-584-3p. Cell proliferation and migration assays showed that miR-584-3p may inhibit the HCC progression. Moreover, we found that the miR-584-3p inhibitor could reverse the effects of LINC00607 downregulation in HCC through rescue experiments. Through verification, miR-584-3p bound to the 3' UTR of ROCK1 to downregulate its expression. CONCLUSION: LINC00607 regulated by MYC can promote the proliferation, migration and invasion of HCC cells through the miR-584-3p/ROCK1 axis.

A Comparison of Elevation, Perforation Rate, and Time Spent for the Crestal Sinus Elevation Intervened by Piezosurgery, CAS-Kit, and Osteotome in a Novel Goat Model.

Purpose: This study aimed to compare the differences among Piezosurgery, CAS-kit, and Osteotome regarding safe elevation, perforation rate, and time spent and to observe and analyze different sinus lifting efficacy of the three methods. Materials and Methods: Twenty-one fresh goat heads (42 sinuses) were investigated. CBCT images confirmed the feasibility of the goat model. The maxillary sinus was successively lifted to 5, 7, and 9 mm by Piezosurgery, CAS-kit, and Osteotome until the sinus membrane was perforated or lifted to 9 mm. In the end, final elevation, sinus perforation, and time spent were recorded. Results: Piezosurgery and CAS-kit lifted sinuses to relatively higher heights than did Osteotome (P = 0.000). Perforation rates (14.29, 21.43%) of the Piezosurgery and CAS-kit were far lower than that of the Osteotome (85.71%). In the Osteotome group, the time of lifting to 9 mm was significantly shorter than that of Piezosurgery and CAS-kit (P = 0.000). There was no statistical difference in time spent between the latter two (P = 0.115). Conclusions: The lifting height of the Osteotome was limited, but it took the shortest time for sinus lifting. Piezosurgery and CAS-kit had higher lifting heights and lower perforation rates compared with Osteotome.

IFP35 as a promising biomarker and therapeutic target for the syndromes induced by SARS-CoV-2 or influenza virus.

Previous studies have shown that the high mortality caused by viruses such as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and influenza virus primarily results from complications of a cytokine storm. Therefore, it is critical to identify the key factors participating in the cytokine storm. Here we demonstrate that interferon-induced protein 35 (IFP35) plays an important role in the cytokine storm induced by SARS-CoV-2 and influenza virus infection. We find that the levels of serum IFP35 in individuals with SARS-CoV-2 correlates with severity of the syndrome. Using mouse model and cell assays, we show that IFP35 is released by lung epithelial cells and macrophages after SARS-CoV-2 or influenza virus infection. In addition, we show that administration of neutralizing antibodies against IFP35 considerably reduces lung injury and, thus, the mortality rate of mice exposed to viral infection. Our findings suggest that IFP35 serves as a biomarker and as a therapeutic target in virus-induced syndromes.

Long non-coding RNA CCDC183-AS1 acts AS a miR-589-5p sponge to promote the progression of hepatocellular carcinoma through regulating SKP1 expression.

BACKGROUND: Hepatocellular carcinoma (HCC) is a common type of malignant human cancer with high morbidity and poor prognosis, causing numerous deaths per year worldwide. Growing evidence has been demonstrated that long non-coding RNAs (lncRNAs) are closely associated with hepatocarcinogenesis and metastasis. However, the roles, functions, and working mechanisms of most lncRNAs in HCC remain poorly defined. METHODS: Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression level of CCDC183-AS1 in HCC tissues and cell lines. Cell proliferation, migration and invasion ability were evaluated by CCK-8 and transwell assay, respectively. Animal experiments were used to explore the role of CCDC183-AS1 and miR-589-5p in vivo. Bioinformatic analysis, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to confirm the regulatory relationship between CCDC183-AS1, miR-589-5p and SKP1. RESULTS: Significantly upregulated expression of CCDC183-AS1 was observed in both HCC tissues and cell lines. HCC patients with higher expression of CCDC183-AS1 had a poorer overall survival rate. Functionally, overexpression of CCDC183-AS1 markedly promoted HCC cell proliferation, migration and invasion in vitro and tumor growth and metastasis in vivo, whereas the downregulation of CCDC183-AS1 exerted opposite effects. MiR-589-5p inhibitor counteracted the proliferation, migration and invasion inhibitory effects induced by CCDC183-AS1 silencing. Mechanistically, CCDC183-AS1 acted as a ceRNA through sponging miR-589-5p to offset its inhibitory effect on the target gene SKP1, then promoted the tumorigenesis of HCC. CONCLUSIONS: CCDC183-AS1 functions as an oncogene to promote HCC progression through the CCDC183-AS1/miR-589-5p/SKP1 axis. Our study provided a novel potential therapeutic target for HCC patients.

Long noncoding RNA SNHG14 promotes hepatocellular carcinoma progression by regulating miR-876-5p/SSR2 axis.

BACKGROUND: Aberrant expressions of long noncoding RNAs (lncRNAs) have been demonstrated to be related to the progress of HCC. The mechanisms that SNHG14 has participated in the development of HCC are obscure. METHODS: Quantitative real-time PCR (qRT-PCR) was used to measure the lncRNA, microRNA and mRNA expression level. Cell migration, invasion and proliferation ability were evaluated by transwell and CCK8 assays. The ceRNA regulatory mechanism of SNHG14 was evaluated by RNA immunoprecipitation (RIP) and dual luciferase reporter assay. Tumorigenesis mouse model was used to explore the roles of miR-876-5p in vivo. The protein levels of SSR2 were measured by western blot assay. RESULTS: In this study, we demonstrated that SNHG14 was highly expressed in HCC tissues, meanwhile, the elevated expression of SNHG14 predicted poor prognosis in patients with HCC. SNHG14 promoted proliferation and metastasis of HCC cells. We further revealed that SNHG14 functioned as a competing endogenous RNA (ceRNA) for miR-876-5p and that SSR2 was a downstream target of miR-876-5p in HCC. Transwell, CCK8 and animal experiments exhibited miR-876-5p inhibited HCC progression in vitro and in vivo. By conducting rescue experiments, we found the overexpression of SSR2 or knocking down the level of miR-876-5p could reverse the suppressive roles of SNHG14 depletion in HCC. CONCLUSION: SNHG14 promotes HCC progress by acting as a sponge of miR-876-5p to regulate the expression of SSR2 in HCC.

Synergistic antioxidant effects of phenolic acids and carotenes on H2O2-induced H9c2 cells: Role of cell membrane transporters.

Phenolic acids (caffeic acid, p-coumaric acid,) and carotenes (ß-carotene, lycopene) were mixed in different ratios to investigate antioxidant interactions on H2O2-induced H9c2 cells with ezetimibe (inhibitor of carotenes membrane transporters). Cellular uptake of carotenes, expression of membrane transporters, reactive oxygen species (ROS), nuclear factor erythroid 2-related factor 2 (Nrf2), NAD(P)H dehydrogenase quinone1 (NQO1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC) were analyzed. Results revealed that phenolic acids increased cellular uptake of carotenes and expression of their membrane transporters. Combination groups contained more phenolic acids showed synergistic effects. For example, ß-carotene: caffeic acid = 1:2 significantly suppressed the intracellular ROS (+EZT, 66.34 ±â€¯51.53%) and enhanced the accumulation of nucleus-Nrf2 (+EZT, 30.23 ±â€¯5.30) compared to the groups contained more ß-carotene (+EZT, ROS: 75.48 ±â€¯2.55%, nucleus-Nrf2: 19.48 ±â€¯4.22). This study provided an implication of functional foods formulation and demonstrated that antioxidant synergism may due to the up-regulation of carotenes membrane transporters by phenolic acids.

Consumption of Interesterified Medium- and Long-Chain Triacylglycerols Improves Lipid Metabolism and Reduces Inflammation in High-Fat Diet-Induced Obese Rats.

Medium- and long-chain triacylglycerols (MLCTs) were synthesized from rapeseed oil (RO), one kind of commonly used edible long-chain triacylglycerols (TGs), and then delivered to high-fat diet (HFD)-induced obese rats. Compared with RO, MLCT consumption exhibited more potent effects on reducing body and tissue weight gains, plasma TG, and total cholesterol (TC) levels and on improving hepatic TG, TC, fatty acid synthase, acetyl-CoA carboxylase, and lipoprteinlipase contents. Meanwhile, lower amounts of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1, and endotoxin in plasma, lower levels of interleukin-6 and TNF-α, and higher levels of interleukin-10 in both livers and white adipose tissues were detected in MLCT-fed rats. MLCT intake also remarkably suppressed the size of adipocytes and the number of macrophages. In conclusion, our study suggested that the interesterified MLCT was more efficacious in improving the lipid metabolism and inflammation in HFD-induced obese rats than RO.

Effects of diacylglycerol and triacylglycerol from peanut oil and coconut oil on lipid metabolism in mice.

Different chain lengths diacylglycerols (DAG) (long- and medium-chain) were synthesized from peanut and coconut oils. The effects of DAG with different chain lengths on body fat, blood lipids, and lipid metabolism-related enzymes in the liver and adipose tissue of C57BL/6J mice were investigated. Compared to peanut and coconut oils containing triacylglycerol (TAG), DAG-rich oils can significantly reduce the body weight, kidney weight, serum triglyceride (TG) content, hepatic fatty acid synthase (FAS), and Acetyl-CoA carboxylase (ACC) enzyme levels (p < 0.05) in C57BL/6J mice. Therefore, the effect of coconut oil DAG on improving body fat metabolism was probably due to the impact of DAG. Meanwhile, the body weight and serum TG content in coconut oil DAG group were lower than those in peanut oil DAG group. In addition, the spleen weight, hepatic ACC, and lipoprotein lipase (LPL) enzymes in coconut oil DAG group (0.07 ± 0.01 g, 2.08 ± 0.42 ng/mg pro, and 18.44 ± 5.23 ng/mg pro, respectively) were significantly lower than those in peanut oil DAG group. Although coconut oil DAG and peanut oil DAG have different fatty acid compositions, their effects on lipid metabolism showed no significant changes. Coconut oil DAG (peanut oil DAG) showed the improved lipid metabolism than that of coconut oil (peanut oil), which was probably due to the effect of DAG. PRACTICAL APPLICATION: Peanut and coconut oils are common edible oils. The oil containing DAG synthesized decreased the body weight and lipid accumulation in mice. Coconut oil is rich in medium-chain fatty acids, while peanut oil mainly consists of long-chain fatty acids. Due to the different contents of fatty acids, the synthesized structural lipids have different effects on lipid metabolism. Medium-chain triglycerides were considered as agents to alleviate obesity.

Investigation of amino acids and minerals in Chinese breast milk.

BACKGROUND: The nutrients in human milk, particularly amino acids and minerals, are important for infant growth and development. Since there are few reports of amino acids and minerals in Chinese breast milk, we conducted this study to establish a representative preliminary database of breast milk nutrients in Chinese breast milk. In this study, we collected breast milk from healthy mothers in seven cities in western, southern and central China. The composition, content and proportion of total amino acids and ten elements (potassium, sodium, calcium, magnesium, iron, zinc, manganese, copper, selenium and phosphorus) in human milk in different lactation stages were investigated. RESULTS: In this study, it was found that the content of total essential amino acids (671.47 mg 100 mL-1 ) in Chinese breast milk was higher compared with the European Society for Paediatric Gastroenterology Hepatology and Nutrition (ESPGHAN) (574 mg 100 mL-1 ), but the content of leucine (LEU) (129.01 mg 100 mL-1 ) and cysteine (CYS) (20.31 mg 100 mL-1 ) was much lower than that recommended by ESPGHAN. Moreover, it was found that the content of most of these ten elements decreased during lactation, and the content of calcium in Chinese breast milk was lower compared with ESPGHAN. In addition, the content of selenium (7.23-20.55 mg 1000 mL-1 ) in breast milk from the three cities Nanchang, Shanghai and Guangzhou in China was much higher than that recommended by ESPGHAN. CONCLUSIONS: In a word, amino acids and minerals in Chinese human milk showed a significant difference from other countries. Human milk meal or infant food should be regulated to meet the requirements of the infant and to maintain the balance of the amino acids and minerals. © 2020 Society of Chemical Industry.

Orbitides isolated from flaxseed induce apoptosis against SGC-7901 adenocarcinoma cells.

Unique plant-derived cyclic peptides family exhibiting various key biological activities has great possibility for anticancer therapy. In this study, we investigated the effects of orbitides isolated from flax (Linum usitatissimum L.) on the growth of SGC-7901 cancer cells and the potential mechanism. Results showed that flaxseed orbitides killed off cancer cells by inducing apoptosis in a dose-dependent manner, which was confirmed by the appearance of nuclear shrinkage and DNA fragmentation, and the inhibitory effect was stronger than that of pure orbitide [1-9-NαC]-linusorb B2 or [1-9-NαC]-linusorb B3. Besides, the mitochondrial apoptosis pathway-related protein cytochrome C (Cyt C) was released from mitochondria to cytosol, associated with the activation of caspases 9 and 3, and the cleavage of PARP. Taken together, these results indicated that flaxseed orbitides induced apoptosis via the mitochondrial pathway, releasing Cyt C, increasing Bax/Bcl-2 ratio and elevating the expression of cleaved caspase 9 and 3 in SGC-7901 cells.

Type-2 11ß-hydroxysteroid dehydrogenase promotes the metastasis of colorectal cancer via the Fgfbp1-AKT pathway.

Type-2 11ß-hydroxysteroid dehydrogenase (HSD11B2) is a key enzyme which converts cortisol to inactive cortisone and is involved in tumor progression and metastasis. Several studies have shown that the promotion of tumor progression and metastasis by HSD11B2 resulted from its physiological function of inactivating glucocorticoids (GC). However, the underlying molecular mechanisms by which HSD11B2 drives metastasis, in addition to inactivating GC, are still unclear. In our study, a series of in vivo and in vitro assays were performed to determine the function of HSD11B2 and the possible mechanisms underlying its role in CRC metastasis. mRNA transcriptome array analysis was used to identify the possible downstream targets of HSD11B2. We found that the ectopic expression of HSD11B2 significantly promoted the migration, invasion and metastasis of colorectal cancer (CRC) cells both in vitro and in vivo, while it did not affect their proliferation in either case. Mechanically, HSD11B2 appeared to enhance cell migration and invasion by upregulating the expression of fibroblast growth factor binding protein 1 (Fgfbp1), and subsequently increasing the phosphorylation of AKT. Furthermore, AKT activation partially mediated the increased expression of Fgfbp1 induced by HSD11B2. HSD11B2 expression was positively correlated with Fgfbp1 and p-AKT expression in clinical samples of CRC. Additionally, knockdown of either Fgfbp1 or AKT impaired the migration and invasion capability of CRC cells with HSD11B2 overexpression, suggesting that HSD11B2 promoted the migration, invasion and metastasis of CRC cells via the Fgfbp1-AKT pathway. Therefore, targeting HSD11B2 or Fgfbp1 may be a novel treatment strategy for inhibiting the metastasis of CRC.

DEPTOR induces a partial epithelial-to-mesenchymal transition and metastasis via autocrine TGFß1 signaling and is associated with poor prognosis in hepatocellular carcinoma.

BACKGROUND: DEPTOR is an endogenous inhibitor of mTORC1 and mTORC2 that plays a vital role in the progression of human malignances. However, the biological function of DEPTOR in HCC metastasis and the underlying molecular mechanisms are still unclear. METHODS: Western blot analysis and immunohistochemistry(IHC) were employed to examine DEPTOR expression in HCC cell lines and tissues. A series of in vivo and in vitro assays were performed to determine the function of DEPTOR and the possible mechanisms underlying its role in HCC metastasis. RESULTS: We found that DEPTOR was frequently overexpressed in HCC tissues, and its high expression was associated with high serum AFP levels, increased tumor size, vascular invasion and more advanced TMN and BCLC stage, as well as an overall poor prognosis. Functional experiments demonstrated that DEPTOR silencing inhibited the proliferation and mobility of HCC cells in vitro and suppressed tumor growth and metastasis of HCC cells in vivo. Accordingly, DEPTOR overexpression promoted the invasion and metastasis of HCC cells in vitro and in vivo, but had no effect on cell proliferation in vitro. Overexpression of DEPTOR induced EMT by snail induction. Conversely, knockdown of snail expression impaired the DEPTOR-induced migration, invasion and EMT of HCC cells. Furthermore, we found that the increase of snail expression by DEPTOR overexpression was due to an activation of TGF-ß1-smad3/smad4 signaling possibly through feedback inhibition of mTOR. CONCLUSION: DEPTOR promotes the EMT and metastasis of HCC cells by activating the TGF-ß1-smad3/smad4-snail pathway via mTOR inhibition. Therefore, targeting DEPTOR may be an ideal treatment strategy for inhibiting the growth and metastasis of HCC.

Lipid Rafts Promote trans Fatty Acid-Induced Inflammation in Human Umbilical Vein Endothelial Cells.

The effects of two fatty acids, oleic acid (OLA) and elaidic acid (ELA) on normal human umbilical vein endothelial cells (HUVEC) and non-rafts HUVEC were investigated in this study. The expression levels of inflammatory cytokines (ICAM-1, VCAM-1 and IL-6) were analyzed. Western blot was used to analyze the expression levels of inflammation-related proteins (NF-κB, ERK1/2) and toll-like receptors 4 (TLR4). The results showed that the levels of nuclear translocation of NF-κB p65 and phosphorylated ERK1/2 were significantly decreased only in non-lipid rafts cells pretreated with trans fatty acid (TFA). The expression of TLR4 in the ELA-treated normal cells was higher than that in non-lipid rafts HUVEC. When the lipid rafts was destroyed by methyl-ß-cyclodextrin, the levels of nuclear translocation of NF-κB p65, phosphorylated ERK1/2 and TLR4 were decreased significantly. Therefore, lipid rafts may be involved in TFA induced-inflammation in HUVEC through blocking the inflammatory signal pathway. Lipid rafts might be a platform for specific receptors such as TLR4 for TFA to activate the pro-inflammation on cell membranes.

Lipid rafts and Fas/FasL pathway may involve in elaidic acid-induced apoptosis of human umbilical vein endothelial cells.

Our previous study showed that trans-fatty acids can cause apoptosis of endothelial cells through the caspase pathway and the mitochondrial pathway. The objective of this study was to explore how trans-fatty acids activate the caspase pathway, whether there exist specific receptors induced apoptosis by comparing normal cells and non-rafts cells treated with elaidic acid (9t18:1) and oleic acid (9c18:1), respectively. Compared to normal cells treated with 9t18:1, the cell viability increased by 13% and the number of apoptotic cells decreased by 3% in non-rafts cells treated with 9t18:1 (p < 0.05), and the expression levels of pro-apoptotic proteins such as caspase-3, -8, -9, Bax, and Bid decreased, and expression of antiapoptotic protein Bcl-2 increased (p < 0.05). In addition, Fas/FasL expression in cell membrane decreased significantly (p < 0.05). In conclusion, the lipid rafts and Fas/FasL pathway may involve in 9t18:1-induced apoptosis of human umbilical vein endothelial cells.

Qualitative and quantitative analysis of phenolics in Tetrastigma hemsleyanum and their antioxidant and antiproliferative activities.

The phenolic profiles of Tetrastigma hemsleyanum leaf extracts by different solvents (80% methanol, ethyl acetate and hexane) and their antioxidant and antiproliferative activities were investigated. Thirteen phenolic compounds (3-caffeoylquinic acid, 5-caffeoylquinic acid, 1-caffeoylquinic acid, 5-p-coumaroylquinic acid, isoorientin-2″-O-rhamnoside, isoorientin, orientin-2″-O-rhamnoside, orientin, 1-p-coumaroylquinic acid, vitexin-2″-O-rhamnoside, isovitexin-2″-O-rhamnoside, vitexin and isovitexin) were identified in T. hemsleyanum leaves for the first time, and six of them were quantified using a combination of LC-QTOF-MS and LC-QqQ-MS techniques. It was found that 80% methanol extract exhibited the highest antioxidant activities (DPPH, 3.32 mmol of Trolox/g DW; ABTS, 1.38 mmol of Trolox/g DW; FRAP, 1.85 mmol of FeSO4/g DW), while the hexane extract had the lowest (1.23, 0.43 and 0.13, respectively). Total phenolic contents (TPC) of various extracts of T. hemsleyanum leaves ranged from 28.95 to 275.71 mg of GAE/g DW. Also, total antioxidant activities as evaluated by ABTS, FRAP and DPPH assays were correlated well with TPC. In addition, 80% methanol extract provided antiproliferative activity on HepG2 cells (IC50 = 524 µg/mL). This paper provides a complete picture of phenolics in T. hemsleyanum leaves and relates them to their antioxidant and antiproliferative activities.

Characterization of medium-chain triacylglycerol (MCT)-enriched seed oil from Cinnamomum camphora (Lauraceae) and its oxidative stability.

Medium-chain triacylglycerol (MCT)-enriched oil was extracted by supercritical fluid extraction of carbon dioxide (SFE-CO(2)) from Cinnamomum camphora seeds. The SFE-CO(2) process was optimized using the Box-Behnken design (BBD). The maximum oil yield (42.82%) was obtained under the optimal SFE-CO(2) conditions: extraction pressure, 21.16 MPa; extraction temperature, 45.67 °C; and extraction time, 2.38 h. Subsequently, the physicochemical characteristics, fatty acid composition, triacylglycerol (TAG) composition, tocopherol content, and DSC profile as well as oxidative stabilities of C. camphora seed oil (CCSO) were studied. Results showed that CCSO contained two major medium-chain fatty acids, capric acid (53.27%) and lauric acid (39.93%). The predominant TAG species in CCSO was LaCC/CLaC (ECN 32, 79.29%). Meanwhile, it can be found that CCSO had much higher oxidative stabilities than coconut oil due to the higher content of tocopherols in CCSO (α-tocopherol, 8.67 ± 0.51 mg/100 g; γ-tocopherol, 22.6 ± 1.02 mg/100 g; δ-tocopherol, 8.38 ± 0.47 mg/100 g). Conclusively, CCSO with such a high level of MCTs and high oxidative stabilities could be potentially applied in special food for specific persons such as weak patients and overweight persons because oils enriched in MCTs can be rapidly absorbed into body to provide energy without fat accumulation.