The effects of propylene glycol mannate sulfate (PGMS) on the lipid peroxide (MDA) , superoxide dismutase (SOD) , glutathion peroxidase (GSH-Px), nitric oxide (NO)and water content in the whole cerebral ischemia/reperfusion injury rabbits induced by four-vessel occlusion,The results show that PGMS can decrease the brain water and MDA, and can increase the SOD and GSH-Px level. No significant effect on the NO level has been detected. The results suggest that the protective effects of PGMS on ischemia/reperfusion injury may be related to its antioxidation.

Guan Xin Shu ( GXS ) is a heparinoid.Quails were randomly divided into 2 groups. All of them were fed with inducer diet containing 1% cholesterol and 20% fat for 6 weeks. 1 group was treated with GXS (200mg/kg/d, ip ) , the other with 0.9% NaCl(0.2ml/100g/d, ip ) . 4 and 6 weeks after administration, serum cholesterol level was significantly reduced (mean 3l%, P

The abnormal proliferation of vascular smooth muscle cells after endothe-lial injury is postulated to be the main pathophysiological process in atherosclerosis (AS). The effects of propylene glycol mannate sulfate(PGMS) on the proliferation of bovine cerebral microvessel smooth muscle cslls (BCMSMCs) induced by 10% fetal calf serum (FCS) and interleukin l(IL-1) were investigated in culture. 5 - 8 stage subcultured BCMSMCs were incubated into 96-well dish- With either 10% FCS or IL-1 (50u/ml) to produce BCMSMCs proliferation , the inhibitory effects of PGMS on proliferation of BCMSMCs were investigated. The results shows that PGMS could inhibit the proliferation of quiescent BCMSMCs induced by 10% PCS. The growth of cells was inhibited, comparing with normal control 72hours after the serum addition as determined by crystal violet stainning and MTTmethod. The proliferation of quiescent BCMSMCs induced by IL-1 (50u/ml) was also inhibited by PGMS as determined by crystal violet stainning and MTT method. The results suggested that PGMS inhibit the proliferation of BCMSMCs induced by 10% FCS and IL-1 ,and the use of PGMS may probably play an important role in the treatment of cerebrovascular disease.

Aim To investigate the effect of low molecular N-trimethyl chloride chitosan(LMTC) on the growth of bovine vascular smooth muscle cells(BVSMCs) in vitro. Methods The antiproliferation activities of LMTC were evaluated in BVSMCs by means of crystal violet staining and MTT assay. The morphological changes of LMTC in BVSMCs were observed under transmission electron microscope. Cell survival ratio influenced by LMTC was assessed by flow cytometer. [WTHZ]Results After BVSMCs were treated by LMTC for 72 h,the growth of the cells was inhibited in vitro and was dependent on concentration; there were some changes of apoptosis by transmission electron microscope and flow cytometer. Conclusion LMTC can inhibit the proliferation of BVSMCs and induce their apoptosis.

This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-α) and activity of nuclear factor kappa B (NF-κB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg·kg-1, iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-α protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptase-polymerase chain reaction (RT-PCR) respectively. NF-κB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-κB α (IκBα) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-α following 2 h of ischemia with 24 h of reperfusion. NF-κB DNA binding activity and the degradation of IκBα in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-α and the activity of NF-κB in rats.

Objective] To amplify,clone and express of a gene encoding hexose transporter of Plasmodium falcipuram(PfHT1) from Southern China isolate FCC1/HN for studing the immune of recombinant which protective from malaria parasite infection. [Methods] Cultivation of P.falciparum isolate FCC1/HN in vitro; extraction of genomic DNA from FCC1/HN using the alkali specific cleavage method; PCR amplification of PfHT1 and cloning into eukaryotic expression vector, pEGFPN3. The recombinant was introduced into mammalian cells, HEPG2 by using liposome\|mediated transfection. [Results] The gene encoding PfHT1 was specifically amplified from the genomic DNA of P.falciparum isolate FCC1/HN. The size of amplified fragment was 1 516 base pair. The eukaryotic expression recombinant, pN3\|HT1 , was constructed and expressed steadily in the hepatocarcinoma cell lines, HEPG2. [Conclusion] The gene encoding PfHT1 was successfully amplified and cloned. The pN3\|HT1/HEPG2 cell line was built for expressing fusion protein of GFP\|HT1.

Objective To screen a new schistosome vaccine candidate. \ Methods\ Schistosoma japonicum adult cDNA library was screened using sera from immune rabbits vaccinated with irradiated cercariae and monoclonal antibodies against membrane antigen of S.japonicum schistosomula. Three different fragments of S.japonicum cDNA genes were cloned into pGEM-T vector. The sequences of the inserts were determined using an automatic DNA sequencer and were analysed using Blast program. One of the unknown genes (B8) was selected and its ORF sequence (291 bp) was subcloned into eukaryotic expression vector. The recombinant plasmids were identified by restrictive enzymes and PCR amplification. The positive recombinant plasmids (pBK/SjB8) were transformed into host bacteria XL1-blue, and were then induced by IPTG for expression. SDS-PAGE and Western blotting analysis of total cellular protein from the bacteria were performed to detect the gene products. Results The results demonstrated that ORF of SjB8 gene was subcloned into the plasmid pBK-CMV and could express as fusion protein in XL1-blue. The results of SDS-PAGE and Western-blot also showed that the molecular weight of the fusion protein with 3 kDa ?-galactosidase was approximately 13\^6 kDa and the actual molecular weights of the SjB8 was 10\^6 kDa. The expressed fusion product of pBK/Sj-B8 could be recognized by immune serum and McAb. Conclusion A new gene of S.japonicum vaccine candidate (SjB8) was cloned into eukaryotic expression vector pBK-CMV and could express 10\^6 kDa schistosome protein. The results provide foundation for further study of the protein for its posibility as candidate vaccine.

Aim To observe the influence of carvedilol on the injury and expression of intercellular adhesion molecule-1 induced by hydrogen peroxide in ECV-304 cells and investigate the anti-atherosclerotic effect of carvedilol.Methods: The viability of ECV-304 cells was detected by MTT assay.Morphological changes of ECV-304 cells were observed under converse microscope.The level of lactate dehydrogenase released to the extracellular medium,the intracellular superoxide dismutase activity and the extracellular and intracellular Malondialdelyde level were determined using automatic biochemistry analyser.The expression of ICAM-1 in protein level and mRNA level was detected with flow cytometric technique and RT-PCR.Results Pretreated with carvidilol(1.0?10~(-5)～1.0?10~(-9)mol?L~(-1)) for 24 h,the cell survival rate was increased significantly in a concentration-dependent manner.Pre-incubation for 24 h with carvedilol results in a significant concentration-dependent decline of LDH release from hydrogen peroxide(1.0?10~(-6)mol?L~(-1))injured cells.While ECV-304 cells were pre-incubated with carvedilol,the level of MDA decreased and the activity of SOD increased significantly.Carvedilol produced a concentration-dependent inhibition of the expression of ICAM-1 protein and mRNA in hydrogen peroxide injured ECV-304 cells in a similar manner.Conclusion: These experiments demonstrated that carvedilol was able to protect ECV-304 cells from the oxidative stress injury and inhibit ICAM-1expression in ECV-304 cells induced by hydrogen peroxide.Therefore,we can consider that carvedilol maintains and improves the function of endothelium damaged by hydrogen peroxide from many aspects,which does indicate extensive antioxidant effects on the hydrogen peroxide-injured vascular endothelial cells and suggest promising effects in atherogenesis process.