From the viewpoint of postmodernism,thinkers believe that the normal form of knowledge has changed from modern-knowledge form to Post-Modernism form.Modern-knowledge form has to face the challenge to its objectivity,generality and value-neutrality.As a result,it has a significant impact on the traditional system of higher education,which leads to another historical reform in higher learning.

OBJECTIVETo investigate the dual role of daphnetin in suppressing high mobility group box-1 protein (HMGB1) release and blocking HMGB1-induced inflammatory response.

METHODSMurine macrophage RAW264.7 cells were cultured in the presence of daphnetin, lipopolysaccharide (LPS), or both. HMGB1 release from the cells was determined using ELISA, and phosphorylations of JAK1/2 and of STAT1 were detected by Western blotting. Human monocytic THP-1 cells exposed to daphnetin, rhHMGB1, or both were examined for NO production using a NO detection kit, for the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and prostaglandin E2 (PGE2) using ELISA, and for expressions of iNOS, COX-2 and phosphorylated p38, ERK, and JNK with Western blotting.

RESULTSDaphnetin dose-dependently reduced the release of HMGB1 in RAW264.7 cells and suppressed rhHMGB1-induced iNOS and COX-2 expressions and release of TNF-α, IL-6, PGE2, and NO in THP-1 cells. Western blotting revealed that daphnetin significantly down-regulated the phosphorylations of JAK-STAT1 pathway in LPS-stimulated RAW264.7 cells but did not suppress the phosphorylations of MAPKs signaling pathway induced by rhHMGB1 in THP-1 cells.

CONCLUSIONDaphnetin can reduce the release of HMGB1 and suppress HMGB1-induced inflammatory response. In RAW264.7 cells, daphnetin inhibited LPS induced HMGB1 release is at least partly mediated by suppressing JAK-STAT1 signaling pathway activation.

Animals ; Cell Line ; Cyclooxygenase 2 ; metabolism ; Dinoprostone ; metabolism ; HMGB1 Protein ; metabolism ; Humans ; Inflammation ; metabolism ; Interleukin-6 ; metabolism ; Janus Kinase 1 ; metabolism ; Lipopolysaccharides ; Macrophages ; drug effects ; Mice ; Monocytes ; drug effects ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type II ; metabolism ; RAW 264.7 Cells ; STAT1 Transcription Factor ; metabolism ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; metabolism ; Umbelliferones ; pharmacology

OBJECTIVEDiscussion on utility and purposed value of obesity and abdomen obesity when body mass index (BMI), waist circumference (WC), waist to hip ratio (WHR) used as indexes predicting hypertension, hyper-blood glucose, and both clusters, to provide scientific basis for the decision on the indexes and their cut-off points of obesity and abdomen obesity in Chinese people.

METHODSUsing the data of diabetes mellitus (DM) from epidemiological studies carried out in 11 provinces/autonomous regions/municipalities of China from July 1995 to June 1997. Partial relative analysis, logistic multi-factors regression analysis, interaction analysis were used. Relative risk (RR), attributable risk proportion (ARP) and population attributable risk proportion (PARP) of hypertension, hyper-blood glucose, and the both cluster as BMI, WC, WHR with the different cut off points were analysed.

RESULTS1) The correlations between BMI, WC and blood pressure, blood glucose were better than the WHR. 2) After adjusted by age, sex, occupation leisure physical activity, education degree and the family history of DM, the results suggested that BMI, WC, WHR were important predictive factors, with relative importance as BMI > WC > WHR. 3) There were augment interactions on BMI, WC and WHR with hypertension, hyper-blood glucose, with the interaction of BMI and WC in particular. Their pure attributable interaction proportion were from 5.95% to 29.34%. 4) The values of RR were about 2.5 when BMI >/= 23, >/= 24 and >/= 25, suggesting the relationship with exposure factors and diseases were with medium and high maleficent extent. Their ARP were from 0.580 to 0.623 with PARP from 0.259 to 0.425. The values of RR were from 2.06 to 3.08 as WC >/= 85 cm in males, WC >/= 80 cm in females while WC >/= 90 cm in males, WC >/= 80 cm in females, which suggested that the relationship with exposure factors and diseases were in medium and high maleficent extent. Their ARP were from 0.515 to 0.676 while PARP from 0.241 to 0.431.

CONCLUSIONSSince the maleficent extent of exposure factors to diseases, the acceptability for overweight and obesity in population, and the prevention and care for overweight and obesity were just in the introduction stage in China. The utility value of predicted hypertension, hyper-blood glucose in BMI and WC seemed to be better then in WHR. We suggested that BMI used as the obesity index, with the diagnostic cut-off point BMI >/= 24. WC as the abdomen obesity index. The diagnostic cut-off points are suggested to be WC >/= 85 cm in males, and WC >/= 80 cm in females.

Adult ; Aged ; Blood Glucose ; metabolism ; Blood Pressure ; physiology ; Body Constitution ; Body Mass Index ; Diastole ; Female ; Humans ; Hyperglycemia ; diagnosis ; physiopathology ; Hypertension ; diagnosis ; physiopathology ; Logistic Models ; Male ; Middle Aged ; Obesity ; physiopathology ; Predictive Value of Tests ; Systole

To investigate the induction of cell cycle arrest of human breast cancer MDA-MB231 cells by Di-indolyl pyrrolidine(DIPRD), a pyrrolidine-derived spirooxindoles compounds. The cytotoxic effect of DIPRD on MDA-MB231 cells was detected by CCK-8 method. The cell cycle arrest of MDA-MB231 cells was detected by DAPI/EdU double-staining. Phosphorylation levels of AKT, mTOR, apoptosis-related proteins p53, MDM2, and DNA repair enzyme PARP levels were detected by Western blot. DIPRD inhibited the viability of MDA-MB231 cells by downregulating the number of EdU-positive cells, increase G1 phase and reduce cell number in S/G2 phase, down-regulated the p-AKT(Ser473), p-mTOR, p-p53, cyclin D1, CDK4, and the upregulated the p-AKT(Thr308), p-MDM2 and Cleaved-PARP levels were detected in a dose-dependent manner at 12. 5, 25, and 50 mg/mL. DIPRD may play a role in cell cycle arrest through AKT signaling pathway and induce cell apoptosis.

OBJECTIVETo study the effect of chrysin in inducing apoptosis of human hepatic carcinoma cells and explore the possible mechanism.

METHODSHuman hepatic carcinoma SMMC-7721 cells treated with DMSO or chrysin at different concentrations (5-200 μg/mL) were examined for changes in the cell proliferation using CCK-8 assay. The morphological changes of SMMC-7721 cells were observed in response to treatment with 5, 10, or 20 μg/mL chrysin, and the changes in the cell nuclei were observed using DAPI nuclear staining. Annexin Ⅴ-FITC/PI flow cytometry was used to determine the cell apoptosis rate. The changes in the apoptosis-related proteins (PARP and caspase-3) and MAPKs signal pathway were detected with Western blotting.

RESULTSChrysin treatment obviously suppressed the proliferation of SMMC-7721 cells in a dose-dependent manner below the concentration of 60 μg/mL. Chrysin (20 μg/mL) also caused significantly increased cell apoptosis and significant cleavage of PARP and caspase-3. Chrysin significantly activated MAPKs signaling pathway in a time-and dose-dependent manner, with the peak activation level occurring at 15 min. Pretreatment of the cells with specific inhibitors of the MAPKs pathway obviously inhibited the effect of chrysin in inducing cell apoptosis.

CONCLUSIONSChrysin inhibits the proliferation and promotes apoptosis of SMMC-7721 cells by regulating the activation of MAPKs signaling.

OBJECTIVE: To explore the role of miR-593 in regulating the proliferation of colon cancer cells and the molecular mechanism. METHODS: Bioinformatics analysis identified PLK1 as the possible target gene of miR-593. Luciferase assay was employed to verify the binding between miR-593 and PLK1, and qRT-PCR and Western blotting were used to verify that PLK1 was the direct target gene of miR-593. CCK-8 assay was performed to test the hypothesis that miR-593 inhibited the proliferation of colon cancer cells by targeting PLK1. RESULTS: Luciferase assay identified the specific site of miR-593 binding with PLK1. Western blotting showed a significantly decreased expression of PLK1 in the colon cancer cells transfected with miR-593 mimics and an increased PLK1 expression in the cells transfected with the miR-593 inhibitor as compared with the control cells ( < 0.05). The results of qRT-PCR showed no significant differences in the expression levels of PLK1 among the cells with different treatments ( > 0.05). The cell proliferation assay showed opposite effects of miR-593 and PLK1 on the proliferation of colon cancer cells, and the effect of co-transfection with miR-593 mimic and a PLK1-overexpressing plasmid on the cell proliferation was between those in PLK1 over-expressing group and miR-593 mimic group. CONCLUSIONS miR-593 inhibits the proliferation of colon cancer cells by down-regulating PLK1 and plays the role as a tumor suppressor in colon cancer.
Binding Sites ; Cell Cycle Proteins ; genetics ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Colonic Neoplasms ; metabolism ; pathology ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; In Vitro Techniques ; MicroRNAs ; genetics ; metabolism ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sincalide ; metabolism ; Transfection