Objective:To investigate whether hydroxytyrosol (HT) may ameliorate oxidative stress and nuclear factor kappa B (NF-?B) activation in the lipopolysaccharide (LPS)-stimulated THP-1 cell line.Methods:The intracellular formation of reactive oxygen species (ROS) was detected by 2,7-dichlorofluorescein diacetate (DCFH-DA) as a fluorescent probe.Intracellular glutathione (GSH) level was estimated by fluorometric methods;Nitric oxide (NO) production was measured as nitrite (a stable metabolite of NO) concentrations.Western blot analysis was used to detect the expressin level of NF-?B.Results:The results showed that treatment of THP-1 cells with HT significantly reduced LPS-stimulated NO production and ROS formation in a concentration-dependent manner.HT at 50 and 100 ?mol/L concentrations increased the GSH level.The specific DNA-binding activities of NF-?B in nuclear extracts from 50 and 100 ?mol/L HT treatments were significantly suppressed.The antioxidant N-acetylcysteine (NAC) also showed the same effects as HT on LPS-induced ROS and NO production,change of GSH level,and NF-?B activation.Conclusion:These findings suggest that HT has antioxidant activity by suppressing intracellular oxidative stress and NF-?B activation in THP-1 cells.

OBJECTIVETo assess the DNA damage of copper 8-quinolinolate (CuQ) and to elucidate the plausible mechanisms.METHODSHepG2 cells were treated with CuQ0-4 μmol·L-1 for different time,DNA damage was measured by Comet assay.Catalase (CAT) activity,glutathione(GSH) level and thiobarbituric acid reactive substances (TBARS) were measured.NF-κB was examined using Western blotting.8-Hydroxydeoxyguanosine (8-OHdG) was measured by immunoperoxidase staining analysis.RESULTSCuQ 0.5 -4 μmol·L-1 caused significant increase of DNA migration in HepG2 cells.CuQ significantly decreased levels of GSH and activity of CAT in HepG2 cells (P ＜0.05).Moreover,CuQ significantly increased accumulation of the p65 subunit of NF-κB into nucleus,levels of lipid peroxidation product TBARS and the formation of 8-OHdG (P ＜0.05).The intracellular GSH level was modulated by pre-treatment with buthionine-(S,R)-sulfoximine (BSO),depletion of GSH in HepG2 cells pre-treated with BSO dramatically increased susceptibility of HepG2 cells to CuQ-induced DNA damage.CONCLUSIONCuQ exerts DNA damage by oxidative stress and increases accumulation of p65 subunit of NF-κB into nucleus in HepG2 cells.

Objective:To explore the prediction model of tissue chip technology for the chemotherapy response of patients with colorectal cancer.Methods:217 patients with colorectal cancer who had received standardized chemotherapy in the Affiliated People’s Hospital of Ningbo University from Jan. 2017 to Dec. 2019 were prospectively selected. The patients were randomly divided into training set (152 cases) and test set (65 cases) according to the ratio of 7:3, and were followed up for 6 months. The clinical data of the patients in the training set were compared, the expression levels of Ang-2, caspase-3 and CD147 in the patients were analyzed by tissue microarray technology, and the related factors affecting the responsiveness of colorectal cancer chemotherapy were analyzed by the Logistic regression model. R software was used based on the training set. A nomogram prediction model was built and model performance on the test set was evaluated.Results:One case was excluded from the training center, and 151 cases were finally included, including 93 cases in the chemotherapy response group and 58 cases in the chemotherapy response group. The tumor diameter, serum carcinoembryonic antigen, caspase3, Ang2 expression level, and the proportion of clinical stage IV in the poor chemotherapy group were significantly higher than those in the good chemotherapy group (all P<0.05) ; Logistic regression showed tumor diameter ( OR=2.394), serum carcinoembryonic antigen ( OR=1.878), caspase-3 ( OR=4.261), Ang-2 expression level ( OR=5.457), and clinical stage IV ( OR=5.954) were independent risk factors for adverse drug reactions in patients with colorectal cancer (all P<0.05). The consistency index (C-index) for predicting the factors related to adverse chemotherapy reactions in patients with colorectal cancer was 0.915. External verification showed that the sensitivity was 86.96%, the specificity was 92.50%, and the accuracy was 90.48% (42/65) . Conclusion:The expression levels of Ang-2 and caspase-3 are correlated with the responsiveness of colorectal cancer to chemotherapy, and can be used as predictive indicators to evaluate the responsiveness of colorectal cancer to chemotherapy.