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.

Objective To investigate the effect of caveolin-1 on rabbit carotid artery anastomotic stenosis and its relationship with TNF-α.Methods 40 New Zealand white rabbits were randomly divided into normal group,surgical group,empty vector group and caveolin-1 transfecting group.Carotid artery end-to-end anastomosis was done in the rabbits except these in normal group.Five specimens were randomly taken on day 7 after surgery for Westem blot to detect the expression of caveolin-1 and TNF-α; The rest specimens were taken for HE staining at fourth week.The ratio of intima/media area were measured by Image-Pro Plus 6.0 software in order to observe the proliferation of intima.Results Compared with normal group,in surgical group intimal proliferation was significant,the intima/media ratio was significantly higher (P ＜ 0.05) ; Compared with surgical group,in caveolin-1 transfected group neointimal proliferation was not obvious,the intima/media ratio decreased (P ＜ 0.05).Western blot showed that:compared with the surgical group,caveolin-1 expression in transfected group was significantly higher (P ＜ 0.05) ; compared with normal group,the TNF-α expression in surgical group increased (t:41.28,P ＜ 0.05) ; Compared with surgical group,TNF-α expression in transfected group decreased significantly (t:36.37,P ＜ 0.05).Conclusions Caveolin-1 inhibits vascular anastomotic stenosis,possibly by down-regulating TNF-α expression.

Objective To investigate the effect of Caveolin-1 on extracellular regulated protein kinases of rabbit carotid artery anastomotic restenosis.Methods 40 New Zealand white rabbits were randomly divided into normal control group,carotid artery end to end anastomosis surgical group,empty vector transfection on the site of anastomosis group and Caveolin-1 transfected group.Left carotid artery endto-end anastomosis was performed,and the mixture of Caveolin-1 plasmid and liposome lipofectin 2000 (transfected group) or empty plasmid and lipofectin 2000 mixture (empty vector group) were transfected on anastomosis.Specimens were taken at 7 d after surgery for Western blot and RT-PCR to detect the expression of protein and mRNA.Specimens were taken for HE staining at 28 d to observe the proliferation of intima,and measured the ratio of intima/media area by Image-Pro Plus 6.0 software.Results Compared with surgical group,the ratio of intima/media area in Caveolin-1 transfected group decreased by about 50％.Compared with surgical group and empty vector group,the Caveolin-1 mRNA expression and protein activity significantly increased (t =36.59,P ＜ 0.01) ; the ERK1/2 mRNA expression and protein activity significantly decreased on rabbit carotid artery anastomotic site in Caveolin-1 transfected group (t =32.64and 7.27,P ＜ 0.01).Conclusions Caveolin-1 inhibits anastomotic restenosis possibly by regulating the activation of ERK.

Objective To evaluate the activation of the visual cortex in patients with primary openangle glaucoma (POAG) and to explore whether the neuronal activity corresponds with retinal nerve fiber layer (RNFL) and cup-to-disc (C/D) values.Methods Twenty-five patients and 25 gender-and agematched healthy volunteers were studied.Blood oxygenation level-dependent functional magnetic resonance imaging (BOLD-fMRI) and three-dimensional brain volume imaging (3 D BRAVO) sequences were obtained using 3 T MR imaging system.A full-screen black-white shift checkerboard was used for visual stimulus during the fMRI experiment and was performed on each eye of all subjects using a visual-acoustical system.All acquired data were postprocessed and analyzed by statistical parametric mapping (SPM).After analysis,individual activated mapping,intra-group mean activated mapping,and inter-group variant mapping were observed.The voxel number,intensity,and Montreal Neurological Institute (MNI) coordinate of the activated clusters were recorded.The Xjviewer software was utilized to obtain activated voxel numbers in occipital lobe.A Pearson correlated test was performed to test the correlation between the number of activated voxels and RNFL,C/D and Hodapp-Anderson-Parrish (HAP) clinical stage.Results Intra-group mean activated mappings of both patients and volunteers showed obvious activation in bilateral occipital lobes.As compared with healthy volunteers,the POAG patients exhibited statistically significantly decreased activation in bilateral occipital lobes,left hippocampus,and left cerebellum,along with lower mean RNFL [(71.56 ±21.54) i m versus (111.88 ± 9.96) μm] and higher C/D values (0.71 ± 0.18 versus 0.36 ± 0.08 ; t value was respectively-10.901 and 11.643,P ＜ 0.05).The number of activated voxels in the occipital lobes of POAG patients did not correlate with RNFL,C/D and HAP clinical stage of the corresponding eye (r value was respectively 0.157,-0.113 and-0.242,P ＞ 0.05).Conclusions fMRI demonstrated differences in visual cortex activation in POAG patients relative to healthy volunteers,suggesting it might be a promising complementary method for diagnosing glaucoma.However,fMRI findings did not correlate with POAG extent,as measured by RNFL and C/D values.Ophthalmological examination remains to play an important role in the evaluation of open-angle glaucoma.