11.0 mmol/L).Perioperative decontamination in digestive tract was a protective factor in the prevention of bacterial infection.Conclusion Bacterial infection is one of the most severe complications after OLT.Therefore,it is very important to remove those risk factors,make early diag- nosis and take effective treatment.

ObjectiveTo investigate the effects of glioma microenvironment and COX-2 inhibitor celecoxib on the phenotypes and function of dendritic cell (DC).MethodsThe expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) production were detected in glioma C6 cells treated with different concentration of celecoxib.Monocytes were isolated from human peripheral blood and cultured with 200 ng/ml rhGM-CSF and 50 ng/ml rhIL-4,either C6 tumor cells supernatant (TSN) or TSN from C6 cells treated with celecoxib to generate DCs.Cell morphology was observed.Cell phenotype including CD1a,CD80,CD83 and D86 were analyzed on a FACScan.Production of IL-12 in DC supernatant and the potential to stmiulate allogeneic T cell proliferation were detected.ResultsThe expression of COX-2 and PGE2 production in C6 cells decreased after treated with celecoxib in a concentration dependant manner.Typical DCs were induced in all groups and the expression of CD1a ((75.56±2.40)％,(75.09±3.67)％,(76.03 ±3.43)％),CD83((72.04±3.45)％,(71.44±3.78)％,( 73.63 ± 3.31 ) ％ ) had no difference (P ＞ 0.05 ).Expression of CD80 ( ( 58.41 ± 3.85 ) ％ ),CD86 ( ( 58.22 ±3.25)％ ) in DC with TSN obviously decreased compared with normal group( (70.36 ± 2.91 )％,(69.31 ±4.29 ) ％,P ＜ 0.01 ) as well as the IL-12 production ( ( 137.88 ± 5.33 ) pg/ml,( 186.04 ± 4.76 ) pg/ml) and the potential to stmiulate allogeneic T cell proliferation ( P ＜ 0.01 ).Celecoxib increased the expression of CD80,CD86 (66.83 ± 2.51,63.51 ± 5.47,P＜ 0.01 ) in DC and the same as IL-12 production( ( 170.31 ± 3.46) pg/ml,P ＜ 0.01 ) and the potential to stmiulate allogeneic T cell proliferation ( P ＜ 0.01 ),which were lower than the normal level.ConclusionGlioma microenvironment may induce the celecoxib can inhibit the expression of COX-2 and PGE2 in gliomas cells and improve the phenotypes and function defect of DCs.

Breast Neoplasms ; genetics ; pathology ; Chromosome Aberrations ; Chromosome Deletion ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 9 ; Female ; Genome, Human ; Humans ; Nucleic Acid Hybridization ; methods ; Phyllodes Tumor ; genetics ; pathology

The DNA structures could be altered or even damaged by exogeous or endogenous factors during cell proliferation. Failure of effective and timely repair will lead to cell cycle arrest or apoptosis. By taking the advantage of the quick proliferation of cancer cells, DNA damage induction, cell cycle arrest and apoptosis promotion have become important strategies for ant-cancer chemotherapy. Previous reports showed that an array of natural compounds inhibit cancer cell proliferation by inducing DNA damage, which have therapeutic potentials for anti-cancer drug research and development.
Animals ; Biological Products ; pharmacology ; therapeutic use ; DNA Damage ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Neoplasms ; drug therapy

AIM: To explore the relationship between the expression of caspase-2 and caspase-3 and the apoptosis in retinal ischemia/reperfusion (I/R) injury of rats, as well as the therapeutic effects of brain derived neurotrophic factor (BDNF)on the ischemic and reperfused retina.METHODS: This experiment was conducted at the laboratory of Affiliated Hospital of Qingdao University Medical College from February 2007 to July 2007. The models of retinal ischemia/reperfusion injury were made by transiently elevating intraocular pressure. A total of 28 rats were divided into Normal and Operative Groups. Operative group was divided into six subgroups. In each subgroup there were four rats. The left eyes of rats were used for I/R and the right eyes were used for intravitreal injection of brain-derived neurotrophic factor (BDNF) as treatment group. After reperfusion we divided our subgroups according to the reperfusion time as 1, 6, 12, 24, 48, 72 hours. The retinal ganglion cell number was counted by using optic microscope(BX-51,Olympus). Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling (TUNEL) method, and the expression of caspase-2,caspase-3 was studied by enzyme linked immunosorbent assay (ELISA) and strept avidin-biotin complex (SABC)immunohistochemistry.RESULTS: No positive apoptotic cells were observed in the normal rats' retinae, but there were a significant number of positive apoptosis cells in 6-24 hours after transient ischemia followed by a decrease at 48 hours. The number of apoptotic cells reached a maximum at 24 hours after ischemia .The expression of caspase-2 gradually increased as early as at 6 hours, reached a peak at 24 hours, then decreased between 48 and 72 hours. Similarly, caspase-3 has the same rule with caspsae-2 in the time courses of expression in retinal tissues.BDNF administered before reperfusion inhibited the expression of apoptosis and ameliorated the retinal tissue damage. It also decreased caspase-2 and caspase-3 expression in ischemic/reperfused retina.CONCLUSION: Retinal ischemia-reperfusion can induce apoptosis of cells in the retina. BDNF rescues retinal ganglion cells (RGCs) from retinal ischemia/reperfusion injury through down-regulation of cell apoptosis and caspase-2 and caspase-3 expression. BDNF have a neuroprotective effect on retina.

nner, reaching peak at a concentration of 30 μmol/L(P < 0. 01). Conclusions RES reduced oxidative stress and apoptosis in an experimental HPLC injury model induced by H2O2. RES plays a key role in the HPLC protection against oxidative injury.

BACKGROUND: Cell-free stem cell therapy has been an issue of concern, but there is no conclusion on how to extract high-quality exosomes. OBJECTIVE: To extract exosomes from human umbilical cord mesenchymal stem cells by using three different methods, and then to screen the optimal method. METHODS: Exosomes were extracted from human umbilical cord mesenchymal stem cells by using the Total Exosome Isolation test kit, Exo Quick test kit and differential ultracentrifugation method, respectively. Then, transmission electron microscopy was used for morphological observations, BCA was utilized to quantify the protein, and western blot assay was applied to detect surface markers CD9, CD81 and CD63. RESULTS AND CONCLUSION: Extraction of exosomes was completed by all the three methods, and round or oval membranous vesicles were observed under the transmission electron microscope. The protein content and purity of exosomes was highest in the differential ultracentrifugation group, followed by the Exobiology Quick kit group, and lowest in the Total Exosome Isolation kit group, and there were significant differences among the three groups (P < 0.05). Under the same protein concentration, surface specific markers, CD81, CD63 and CD9, were expressed highest in the differential ultracentrifugation group, followed by the Exobiology Quick kit group, and lowest in the Total Exosome Isolation kit group. The operating time was significantly lower in the Exobiology Quick kit group compared with the other two groups (P < 0.05). To conclude, despite a longer operating time, the differential ultracentrifugation method is a rational method to extract enough exosomes with relative high purity.

OBJECTIVETo study the effect of folic acid cooperating with soybean isoflavone on the oxidative status of neural tube defects (NTDs) pregnant rats induced by cyclophosphamide, to observe the relationship of the two factors, folic acid and the isoflavone and to look for the best co-intervention group.

METHODSThe 100 pregnant rats of 2.5-3 months old were randomly divided into the control group, model group, co-intervention groups and solo-intervention groups. The animals were executed on the 20th day of gestation as to examining the levels of antioxidative indices (GSH, GSH-Px, Se, Mn, Fe) in blood. The incidence rates of NTDs were calculated.

RESULTSThe interaction of folic acid and isoflavone had significant effect on the indices related with antioxidation (P < 0.05). Folic acid 0.7 mg/kg cooperated with isoflavone 160 mg/kg had the best intervention effects in our study. Compared with the solo-intervention by folic acid 1.4 mg/kg and isoflavone 320 mg/kg, the effect of co-intervention (folic acid 0.7 mg/kg cooperated with isoflavone 160 mg/kg) was significantly better (P < 0.05).

CONCLUSIONFolic acid should be the main protective factor of NTDs, and isoflavone might reinforce the protective effects of folic the acid on NTDs by increasing the antioxidative ability, however, the effect is related with the ratio of the two factors.

Animals ; Cyclophosphamide ; Drug Interactions ; Female ; Folic Acid ; pharmacology ; Isoflavones ; pharmacology ; Male ; Neural Tube Defects ; chemically induced ; prevention & control ; Pregnancy ; Rats ; Rats, Wistar ; Soybeans ; chemistry

AIMTo explore the changes of MMP-2/9 protein expression and excitation in brain of repetitive hypoxic mice.

METHODSThe biochemistry techniques of SDS-PAGE, Western bolt and Gel Goc Image Analysis System were applied to determine the level of MMP-2 and MMP-9 expression and activation in cortex and hippocampus of mice. The animals were randomly divided into 5 groups: the normal control group (H0), acute hypoxic (H1, hypoxic exposure once), repetitive hypoxic groups (H2-H4, repetitive hypoxia for 2-4 runs respectively).

RESULTS(1) The MMP- 2 expression level was increased first then decreased in hippocampus and the significant decrease was found in H4 group (P < 0.05, n=6), but no significant changes among the 5 groups in cortex. In addition, no activated form of 66 kD MMP-2 had been detected both in hippocampus and cortex. (2) Along with the development of brain hypoxic preconditioning, the level MMP-9 protein expression also increased first then decreased gradually in hippocampus, and the significant changes were found both in H1 and H4 groups (P < 0.05, n=7 for each group). The same trace of changes was also found in the activation of MMP-9 (include 82 and 78 kD forms) in hippocampus, and the significance both in H1 and H4 (P < 0.05, n=7 for each group) were detected. However, there was not any significant change in the level of MMP-9 protein expression or activation to be found in cortex.

CONCLUSIONThese results suggested that MMP-2 and MMP-9 might play certain role in the development of cerebral hypoxic preconditioning, the different changes of MMP-2/9 protein expression and activation both in cortex and hippocampus might be involved in their selective vulnerability to hypoxia.

Animals ; Hypoxia, Brain ; metabolism ; Ischemic Preconditioning ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Mice ; Mice, Inbred BALB C

OBJECTIVETo investigate the effects of microwave radiation on thymocytes in mice at different power densities.

METHODSThe experimental animals were whole-body exposed to microwave radiation with frequency of 2,450 MHz, power density of 1, 5, 15 mW/cm(2) respectively 1 h everyday for 30 days. Then the thymus were taken out after the mice were decapitated. Thymus index, morphological characteristics of thymus were examined. The changes of thymus T-cell subgroups, cell cycle progression in thymocytes and cellular apoptosis were detected with flow cytometry (FCM).

RESULTSThe body weights of animals in 5, 15 mW/cm(2) irradiation groups [(28.10 +/- 1.46), (27.50 +/- 2.52) g] were lower than that of the control [(31.95 +/- 2.51) g] (P < 0.05). Pathological observation showed dark red piece of nucleus, some nuclei inclined to one side, slight increase in hassall body. The expressions of CD8 in 5, 15 mW/cm(2) irradiation groups (29.14% +/- 1.68%, 29.18% +/- 0.81%) were higher than that in control group (26.95% +/- 1.27%) (P < 0.05). The percentages of G(2) + M phase thymocytes in both radiation groups (12.24% +/- 1.82%, 11.19% +/- 1.36%) were lower than that in control group (14.58% +/- 0.64%) (P < 0.01). Thymocytic apoptosis rates in the three experimental groups (7.18% +/- 0.99%, 10.06% +/- 1.58%, 9.45% +/- 0.92%) were higher than that in control (4.25% +/- 1.63%) (P < 0.01), but the evident difference between 5 mW/cm(2) and 15 mW/cm(2) was not found (P > 0.05).

CONCLUSIONSub-chronic microwave exposure (2 450 MHz, 5, 15 mW/cm(2)) could induce thymocyte apoptosis, cause pathological changes in thymus, and affect cell cycle progression, thus may inhibit the immune function of the animal.

Animals ; Apoptosis ; radiation effects ; Dose-Response Relationship, Radiation ; Female ; Male ; Mice ; Microwaves ; adverse effects ; T-Lymphocytes ; radiation effects ; Thymus Gland ; cytology ; radiation effects