The changes of plasma Fn content in rabbits of hemorrhagic and endotoxic shock has been assayed by means of single and double immunodiffusion tests. The results showed that Fn level significantly declined at 30 minutes after hemorrhagic shock and remained at low level with development of shock. But in the rabbitns transfused at 30 minutes after shock Fn level turned to normal as blood pressure increased. Fn content was significantly elevated at 30 minutes and significantly decreased at 60 minutes after endotoxic shock. The possible pathophysiologic and clinical significance of these changes was disscussed.

AIM: To study the apoptotic effect of TNFα on rat pulmonary microvascular endothelial cells (PMVEC) and the influences of Fas, NF-κB in its mechanism. METHODS: Apoptosis of PMVEC was analyzed and quantitated with TUNEL, flow cytometer. The distribution of NF-κB was detected via histoimmunochemical staining in TNF-treated cells and the control. Northern blot was applied to assess the influence of TNF on PMVEC Fas expression. Fas antibody was used to investigate the apoptotic effect of Fas on PMVEC. Activation of caspase-8 was detected with Western blot. Expression of caspase-3 was analyzed with histoimmunochemical staining. RESULTS: After treatment with 5×108 U/L TNF for 24 hours, viable PMVEC significantly diminished. Apoptosis rate was 14.0%±3.1% detected with TUNEL, and 13.1% with flow cytometer. Histoimmunochemical staining showed that NF-κB relocated from cytoplasm to the nuclear. When the cells were co-cultured with TNF and APDC, an NF-κB inhibitor, less cells were viable and more cells were positively stained with TUNEL. Fas expression in PMVEC was elevated treated with TNF. Apoptosis in PMVEC was found aggravated, when the cells were co-cultured with TNF and anti-Fas antibody. The positive rate was 24.1%±1.5% with TUNEL. Increase of caspase-8 activation was manifested by Western blot following TNF stimulation. Caspase-3 expression was found elevated using histoimmunochemical staining. Cell permeable caspase-3 inhibitor significantly ameliorated PMVEC apoptosis induced by TNF. CONCLUSION: 1. Large dose of TNF(5×108 U/L) can induce apoptosis in rat PMVEC. 2. NF-κB has a protective effect on PMVEC apoptosis. 3. TNF up-regulates Fas expression in PMVEC. And the latter takes a part in apoptosis. 4. TNF induced caspase-8 activation in PMVEC, and more caspase-3 was expressed. These may be involved in PMVEC apoptosis induced by TNF.

The phospholipid content in BALL markedly increased (P0.01) in septic rats induced by cecal ligation plus punctures as compared with non-septic control. Meanwhile, the lamellar inclusion bodies in type Ⅱ alveolar epithelial cells were empty observed in electro-microscopic examination. Authors suggest that the changes mentioned above is a compensatory response related to stress in early stage of sepsis.

A Review] Endothelial cells produce both superoxide and nitric oxide. Nitric oxide and superox- ide are known to react rapidly to form the stable peroxynitrite anion. Peroxynitrite mediates the oxidation of protein, lipid, deoxyribose and inhibits mitochondrial electron transport. Peroxynitrite may break DNA strands and activate poly(ADP - ribose) syntheatase. If the reaction is excessive, it results in a depletion of intracelular NAD+ and ATP. There is ultimately cell death.

AIM:To study the apoptotic effect of TNF? on rat pulmonary microvascular endothelial cells (PMVEC)and the role of Fas, NF-?B in its mechanism. METHODS: Apoptosis of PMVEC was analyzed and quantitated with TUNEL, flow cytometer. Northern blot was applied to assess the influence of TNF? on PMVEC Fas expression. Fas antibody was used to investigate the apoptotic effect of Fas on PMVEC. Activation of caspase-8 was examined by Western blot. Expression of caspase-3 was analyzed with histo-immunochemical staining. RESULTS:Growth curve showed that TNF? suppressed endothelial cell proliferation in a dose-dependent manner. After treatment with 5?10 6 U/L TNF?, apoptotic rate was 14.0%?3.1% detected with TUNEL, and 13.1% with flow cytometer. When the cells were co-cultured with TNF? and APDC, an NF-?B inhibitor, less cells were viable and more cells were positively stained with TUNEL. Fas expression in PMVEC was elevated after TNF? treatment. Co-culturing with Anti-Fas antibody aggravated PMVEC apoptosis. Caspase-8 activity and caspase-3 expression was elevated. Caspase-3 inhibitor significantly ameliorated PMVEC apoptosis. CONCLUSION: Large dose of TNF? (5?10 6 U/L) can induce apoptosis in rat PMVEC. NF-?B has an anti-apoptotic effect in PMVEC. TNF? up-regulates Fas expression in PMVEC, and the latter takes a part in apoptosis. Caspase-8 and caspase-3 are involved in PMVEC apoptosis induced by TNF?.

Angiopoietin-1 (Ang-1) is a newly-found endothelium-specific proangiogenic factor and it had been proved essential roles in both vasculogenesis and angiogensis. Among them, its anti-leakage ability may have great potential applications in clinical treatment of vascular hyper-permeability in a variety of diseases such as cancer, diabetic retinopathy, rheumatoid arthritis, asthma. In this review, some research progresses focused on this aspect are discussed. [

Thevascularendothelialprogenitorcellsareapopulationoffunctionalendothelialprecur sorsincirculatingblood ,whicharederivedfrombonemarroworcordblood .CD34+,Flk - 1+andACl33+ aretheirmolecularmarkers .Inthisreview ,thefunctionalcharacterizationofvascularendothelialprogenitor cellsisintroducedandtherelationshipbetweenvascularendothelialprogenitorcellsandangiogenesisinis chemiccardiovasculardiseasesisdiscussed .Thesedatamayofferafoundationforthedevelopmentofthera peuticangiogenesisforthepreventionandtreatmentofischemiccardiovasculardiseasesbytransplantationof vascularendothelialprogenitorcells .

Thyptase,a predominant serine protease in mast cells,is released by mast cell degranulation in an enzymatically active form.Recent research suggests that ttyptase plays important roles in mast cell mediated anaphylaxis,angiogenesis,initiation and promotion of neoplasm.This paper reviews tryptase's struture,molecular biology,biochemistry,processing,activation and its relationship with diseases.

AIM: To study the effects of VEGF over-expressed C6 glioma cells on the expression of Flk-1 and Flt-1 in cocultured microvascular endothelial cells using the rat hepatic cells BRL 3A as control. METHODS: Cocultured systems of rat pulmonary microvascular endothelial cells with C6 and endothelial cells with BRL 3A were established. Immunocytochemical method was used to investigate the expression change of Flk-1 and Flt-1 protein in cocultured microvascular endothelial cells. The expression of Flt-1 and Flk-1 mRNA was analyzed by RT-PCR and Northern blot. RESULTS: The microvascular endothelial cells cocultured with C6 showed increased expression of Flk-1 and Flt-1 protein ( P

AIM：To investigate the role of NF-κB in the activation of inducible nitric oxide synthase (iNOS) gene by tumor necrosis factor alpha (TNF α) and lipopolysaccharide (LPS) in endothelial cells and effect of antioxidant on the induction of iNOS. METHODS：Rat pulmonary microvascular endothelial cell (RPMEC) was cultured and the cells were identified with antiendothelial cell antibody CD31 using immunohistochemistry(ABC). The concentration of nitrite in the culture media was determined based on Griess reaction. iNOS mRNA was analyzed using RT-PCR and Northern blot. NF-κB in cell nuclei was detected with electrophoresis mobility shift assay (EMSA). RESULTS：A marked production of nitrite in RPMECs was found after 24 hours treatment with TNF α(105 U/L) and LPS (1 mg/L) (P＜0.01). The level of iNOS mRNA increased significantly after adding TNF α(105 U/L) and LPS (1 mg/L) to the cell media for 2 hours (P＜0.05). Pretreatment with cycloheximide (CHX, 10 mg/L) or antioxidant, PDTC (0.1 mmol/L) or NAC (20 mmol/L) significantly decreased nitrite production and iNOS mRNA expression induced by TNF α(105 U/L) and LPS (1 mg/L) (P＜0.05). Furthermore, there was a dose-effect relationship between PDTC/NAC and inhibitory effect. TNF α (105 U/L) and LPS (1 mg/L) triggered the activation and translocation of NF-κB. This effect was blocked by adding PDTC (0.1 mmol/L) or NAC (20 mmol/L) to the cell media for 1.5 hours.CONCLUSION：1.TNFα and LPS may induce iNOS gene expression at transcriptional or posttranscriptional level. The upregulation of iNOS depends on new protein synthesis. 2. The induction of iNOS gene expression by TNFα and LPS is dependent on the activation of NF-κB. 3. Antioxidants may inhibit the induction of iNOS gene through the inhibition of NF-κB activation.