Angiogenesis and invasion are two remarkable features of spongioblastoma,which lead to the failure of clinical treatment.With the development of the glioma（s） molecular biology mechanism in the realm of angiogenesis,some anti-angiogenesis drugs have got a positive therapeutic efficacy in the clinical trials,such as bevacizumab.However,it is reported that these drugs maybe also enhance the invasion and migration ability of glioma cells in the process of anti-angiogenesis therapy.Matrix metalloproteinases,hypoxia induced factor-1 and the inositol-requiring enzyme-1 maybe have some correlations with the change of the invasion and migration,but the molecular biological mechanism needs further research.

The inhibitory effects of total glucosides of Moutan Cortex (TGM) and to talglucosides of Paeony Lactiflora (TGP) on osmotic hemolysis and oxidative hemolysis induced by hydrogen peroxide were studied. TGM at lower concentration and TGP could inhibit osmotic hemolysis significcantly, but higher concentration (100mg ? L-1) of TGM had a hemolytic activity. TGM and TGP could inhibit hemolysis induced by H2O2 significantly,but TGM was more effective than TGP. TGM .TGP and Vit E all could inhibit lipid peroxidation and glutathione depletion, induced by H2O2, on erythrocytes.

The protective effects of total glucosides of paeony (TGP) on eoperimental hepatitis were studied in mice. The elevation of SGPT and the decrese of serum protein and hepatic glycogen contents in D-Galactosamine or CCl4-induced hepatitis were significantly improved by pretreatment with TGP (10, 20mg ? kg-1d-1?7d,ip). It also remarkably diminished the hepato-cellular degeneration and necrosis induced by D-Galactosamine or CCI4.Moreover, ultrastructural studies showed that TGP markedly restored the structures of mitochondria, lysosome and endoplasma reticulum of hepatocvtes injured by D-Galactosamine. These results indicate that TGP has obviously protective effects on acute hepatitis. The mechanisms of its actions remain to be furthes studied.

Humans ; Child ; Face ; China

AIM: To investigate the expression of PPARγ and Nrf2/γ-GCS-h in inflammatory cells in bronchoalveolar lavage fluid(BALF) of guinea pig with bronchial asthma of acute episode, and to explore the roles of PPARγ on Nrf2/γ-GCS-h expression. METHODS: Forty adult male guinea pigs were randomly divided into 4 groups (10 guinea pigs in each group): control group (group A), asthmatic group (group B), dexamethasone treatment group (group C) and rogridone treatment group (group D). The asthmatic model was established by an ovalbumin challenge method. BALF was collected, and the total cell count and the proportion of the inflammatory cells were measured. After centrifugation, the concentrations of ROS and MDA in the clear supernatant were detected. The methods of in situ hybridization and immunohistochemistry were used for detecting the expression of PPARγ and Nrf2/γ-GCS-h at mRNA and protein levels. RESULTS: The proportion of eosinophils (EOS) in BALF in group B was significantly higher than that in groups A, C and D (P<0.01). The concentrations of ROS and MDA in BALF of group B was the highest. The difference of ROS and MDA was statistically significant (all P<0.05) as compared to the control. The results of immunohistochemistry and in situ hybridization indicated that the A value was the lowest in group B as compared to that in groups A, C and D (all P<0.01). In group B, the positive correlations were observed between PPARγ and Nrf2/γ-GCS-h, between γ-GCS-h and Nrf2. A negative correlation between the proportion of EOS in BALF and the expression of PPARγ and Nrf2/γ-GCS-h was also observed (all P<0.05). CONCLUSION: In acute asthmatic models induced by ovalbumin, the expression of PPARγ and Nrf2/γ-GCS-h is decreased, and PPARγ may up-regulate the expression of Nrf2/γ-GCS-h to inhibit the inflammatory and oxidative reactions, indicating a new way for prevention and treatment of bronchial asthma.

AIM: To explore the effects of peroxisome proliferator-activated receptor γ (PPARγ) on the activity and expression of γ-glutamylcysteine synthetase (γ-GCS), and its role in rats with chronic obstructive pulmonary disease. METHODS: COPD model was established by the method of combining fumigation and lipopolysaccharide (LPS) intra-tracheal dripping. Meanwhile, some of the COPD rats were administered with rosiglitazone (RGZ), a PPARγ activator. The pulmonary function and the pathological changes were determined. ROS content and γ-GCS activity in lung tissues were detected. The levels of PPARγ, γ-GCS mRNA and protein expression in lung tissues were measured by immunohistochemistry, Western blotting, in situ hybridization (ISH) and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The pulmonary function (FEV_(0.3), FEV_(0.3)/FVC%, PEF) were significantly improved in RGZ group compared to COPD group. Under light microscope, lung pathological changes in COPD group conformed to pathological features of COPD. The pathological changes of lung tissue were obviously reduced in RGZ group compared to COPD group. In RGZ group, ROS content was obviously reduced and γ-GCS activity significantly increased compared to COPD group. Protein and mRNA expressions of PPARγ and γ-GCS in COPD group significantly higher than those in control group (all P<0.01), and those in RGZ group was markedly increased compared to COPD group (all P<0.05). Linear correlation analysis showed that PPARγ protein was positively correlated with γ-GCS activity (r=0.634, P<0.01), and was no significantly correlated with ROS content (r=0.214, P>0.05). PPARγ protein was positively correlated with γ-GCS protein and mRNA (r=0.553, r=0.442, all P<0.01). CONCLUSION: PPARγ activation by RGZ reduces the extent of COPD oxidant/antioxidant imbalance, which plays an important role in the prevention and treatment of COPD. In addition, PPARγ may play an important antioxidant protection role by reducing ROS production, and increasing activity and gene expression of γ-GCS in the lung.

Stroke is a common neurological diseases with high morbidity,high mortality and high morbidity characteristics,which brings great suffer and economic burden to the patients and families,and has become an important research topic in contemporary medical profession.Treatment directly affects the prognosis of patients with cerebral infarction,and thus it is very important to find the most effective treatments and methods.Currently,thrombolytic therapy in acute cerebral infarction have carried out a large number of experimental studies,and achieved good results.This paper reviewed the thrombolytic therapy in acute cerebral infarctionincluding the time window,methods and drugs of thrombolysis,and the influencing factors of outcomes were also summarized and discussed.

BACKGROUND: Simple polyvinyl alcohol (PVA) has limited ability to cell adhesion. There are not generally accepted studies on improved effects of collagen protein modified polyvinyl alcohol on cell adhesion and proliferation.OBJECTIVE: To investigate the feasibility of PVA/type Ⅰ college (COL-Ⅰ) as anterior cruciate ligament (ACL) scaffolds in tissue engineering.DESIGN, TIME AND SETTING: The controlled observation experiment was performed at the Fourth Affiliated Hospital, Medical College. Ji'nan University, Guangzhou Red Cross Hospital, Guangzhou Institute of Trauma Surgery from August 2006 to October 2007.MATERIALS: COL-Ⅰ gel was produced by Guangzhou Institute of Trauma Surgery.METHODS: PVA filature was used to weave fascicular scaffolds. NIH-3T3 cell line and human ACL cells were in vitro incubated, amplified, and then implanted on the PVA/COL scaffolds.MAIN OUTCOME MEASURES: The growth of NIH-3T3 cell line and human ACL cells on the PVA/COL scaffolds and the secretion of extracellular matrix were observed using scanning electron microscope. Cell compatibility of PVA/COL scaffolds was assessed. Mechanics characteristic of PVA/COL scaffolds was measured by using the electric. tensile force apparatus. Mechanical property of PVA/COL scaffolds was analyzed using the SPSS 11.5 software package.RESULTS: NIH-3T3 cell line and human ACL cells on the PVA/COL scaffolds adhered, proliferated, and secreted extracellular matrix. NIH-3T3 cell line highly grew compared with human ACL cells on the PVA/COL scaffolds. The adhered number of NIH-3T3 cell line and human ACL cells was significantly increased on the PVA/COL scaffolds. NIH-3T3 cell line and human ACL cells presented well morphology on the PVA/COL scaffolds. COL-Ⅰ could promote the secretion of extracellular matrix from NIH-3T3 cells, but its effects on human ACL cells were not significant. Tensile force test showed that load-extension curve of the materials was identical to ACL of human and rabbits, and the scaffolds possessed strong flexibility. The maximal load, ultimate stress and elastic modulus were respectively 52.61 N, 14.96 MPa and 202.08 MPa.CONCLUSION: COL-Ⅰ accelerates the adhesion and proliferation of NIH-3T3 cell line and human ACL cells on the surface and in the pore of the PVA/COL scaffolds, promotes the secretion of extracellular matrix from NIH-3T3, and PVA filature material has mechanical property and good cell compatibility.

Objective To investigate the inhibitory effect of X-linked inhibitor of apoptosis associated factor-1(XAF1) on xenograft growth in nude mice with hepatocellular carcinoma. Methods The models of xenografted nude mice with human hepatocellular carcinoma cell line SMMC7721 were established. Intratumor injection was performed on three tumor sites in each group of mice (n=5) with recombinant adenovirus Ad5/F35-XAF1, control virus Ad5/F35-Null at the same infective titre or PBS of the same volume every two days for two weeks. The volumes of xenografts in all nude mice were measured every three days, and the differences between Ad5/F35-XAF1 group and the other two groups were compared. The apoptosis of tumor cells was determined by in situ end-labeling TUNEL method, the expression of XAF1 protein and microvessel density (MVD) were detected by immunohistochemistry. Results Intratumoral injection of Ad5/F35-XAF1 significantly inhibited the growth of tumor xenografts with smaller tumor size, less tumor weight and lower MVD compared with those injected with control virus Ad5/F35-Null and PBS (P<0.05 or P<0.01). However, the apoptosis index and expression of XAF1 protein in Ad5/F35-XAF1 group were significantly increased compared with the other two groups (P<0.01). Conclusion Ad5/F35-XAF1 significantly inhibits xenograft growth in nude mice with hepatocellular carcinoma, which is probably associated with the effects of XAF1 inducing hepatocellular carcinoma cell apoptosis and suppressing tumor angiogenesis.

Objective To elucidate the expression of gankyrin in human gastric cancer cells and it's role in nimesulide induced apoptosis. Methods Four human gastric cancer cell lines including MKN28 (well differentiated), AGS (poorly differentiated), MKN45 (poorly differentiated), and SGC7901(moderately differentiated) were cultured and treated with nimesulide. Nimesulide induced growth inhibition and apoptosis of the cells were detected by methyl thiazolyl tetrazolium assay, and confirmed by flow cytometry. The expressions of gankyrin gene and protein were further assessed by real-time PCR and Western blotting. Results Gankyrin mRNA and protein were detected in all four human gastric cancer cell lines. The proliferations of AGS and SGC7901 cell lines were significantly suppressed by nimesulide in a time-dose dependent manner. When treated with 400 μmol/L of nimesulide for 48 hours, the significant apoptosis was found in AGS cells (23.30%±2.50%) and SGC7901 cells (16.80%±1.55% ) in comparison with controls (0.57%±0.19% and 0.88%± 0.17%, respectively, all P values <0.01). Apoptosis of AGS cells induced by nimesulide was accompanied by a considerably decreased gankyrin expression that was more significant at 24 hours (0.0035±0.0014) and 36 hours (0.0980±0.0160) in comparison with controls (0.4690±0.1190, all P values<0.01). Conclusion Gankyrin expresses in human gastric cancer cell lines and may be involved in nimesulide induced apoptosis of AGS cells.