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Objective:To observe the affection of angiotensin Ⅱ antagonists on the cultured subtype 2 receptor of angiotensin II transfected aortic vascular smooth muscle cells of rat.Methods:After transfected the plasmid that contained the cDNA of subtype 2 receptor of angiotensin II into cultured rat vascular smooth muscle cells, the cells were divided into three groups：cells of group 1 were treated with angiotensinⅡ,cells of group 2 were treated with angiotensinⅡand losartan,cells of group 3 were treated with angiotensinⅡ and PD123319 .After experiments，the expression of PCNA, NOS and the cell number was tested, respectively.Results：After treated with Losartan，the cell number of group 2 was(4.17±0.15)×105，the OD value of PCNA was 0.202 6±0.007 6，both of which were less than that of cells of group 3；the OD value of NOS of cells was more in group 2(0.027 5±0.002 1 ) than that in group 3 (0.016 9±0.002 0) (P＜0.01).Conclusions:It suggests that when being activated,subtype 2 receptor of angiotensin Ⅱ could inhibit the proliferation of vascular smooth muscle cells and antagonist the effect of subtype 1 receptor of angiotensin Ⅱ,such an effect may be related to the activation of NOS.
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AIM：To analyse sequences of p62dok amino acid and cDNA and to investigate p62dok tyrosine phosphorylation and its relation with p21ras GAP. METHODS：The purified p62dok was extracted from CHO/IR cells. The peptide sequence of p62dok was carried out on a high performance analyzer. PCR was performed with the primers designed from the sequence of p62dok amino acid. Western blot and immunoprecipitation were used to identify tyrosine phosphorylation of p62dok and the binding of p62dok with p21ras GAP. RESULTS：The p62dok cDNA is a 1863 bp sequence and code 481 amino acid with 15 tyrosine residues and a putative pleckstrin homology domain. The p62dok protein is rich in PxxP motif. The tyrosine-phosphorylated p62dok can bind p21ras GAP. CONCLUSION：Perhaps p62dok is a new signaling molecule and play an important role in insulin signaling networks through RAS/MAPK pathway.
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AIM: To observe the effect of protein kinase C-?(PKC?)antisense oligonucleotide on cell growth, cell cycle and the expression of cyclin E in human poor-differentiated nasopharyngeal carcinoma(NPC) cell line CNE-2Z. METHODS: Antisense PKC? was transfected by cationic liposome(LP) in CNE-2Z cells to analyze the cell growth and cell cycle by MTT colorimetric assay and flow cytometry, respectively. Moreover, the expression of cyclin E was determined by immunocellularchemistry and scanning the result of dot-blotting. RESULTS: ①With the concentration of antisense PKC? increasing, the relative cell growth index was decreased gradually( P
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AIM:To analyse sequences of p62 dok amino acid and cDNA and to investigate p62 dok tyrosine phosphorylation and its relation with p21 ras GAP. METHODS:The purified p62 dok was extracted from CHO/IR cells. The peptide sequence of p62 dok was carried out on a high performance analyzer. PCR was performed with the primers designed from the sequence of p62 dok amino acid. Western blot and immunoprecipitation were used to identify tyrosine phosphorylation of p62 dok and the binding of p62 dok with p21 ras GAP. RESULTS:The p62 dok cDNA is a 1863 bp sequence and code 481 amino acid with 15 tyrosine residues and a putative pleckstrin homology domain. The p62 dok protein is rich in PxxP motif. The tyrosine-phosphorylated p62 dok can bind p21 ras GAP. CONCLUSION:Perhaps p62 dok is a new signaling molecule and play an important role in insulin signaling networks through RAS/MAPK pathway.
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The MDA contents, SOD and. GSH-Px activities of the heart, liver, brain, kidney and serum were observed systematically in isoprotercnol-induced myocardial infarction. The results suggested that the MDA contents, SOD and GSH-Px activities were increased in ischemic myocardium. Oxygen free radicals exerted detrimental effects on vitals organs, and also was accompanied by a compensatory increase of SOD and GSH-Px activities.
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Advanced detective methods at present were used to carry out 11 kinds of routine and special tests in 187 patients with epidemic hemorrhagic fever (EHF) who were divided into three groups: DIC, suspected DIC and no DIC group, according to coagulation tests (analysis of platelet count, fibrinogen, prethrombin time, thrombine time and FDP), to study simultaneously that how the systems of coagulation, fibrinolysis, kinin and complement changed in EHF patients with or without DIC. The quantitation of plasminogen activity was first tested in EHF patients in this study.
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AIM To compare the protective effects of norepinephrine preconditioning(NEPC)and ischemic preconditioning(IPC)on myocardial ischemic/reperfused injury in rats in vivo . METHODS Rats were divided into control, ischemia/ reperfusion, classic IPC and NEPC groups. After 20 min reperfusion, several indexes including cardiac function indexes, MDA were tested, the myocardial ultrastr ucture and the injury reaction of catalase observed. RESULTS Both IPC and NEPC could protect myocardial ultra structure, ameliorate left heart function, decrease cardiac MDA content and protect the activity of catalase. CONCLUSION Extra micro norepinephrine preconditioning as a non injury method can mimic the protective effects of classic IPC and shows its clinical values.
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AIM: To observe the effect of angiotensinⅡ subtype 2 receptor (AT_2 receptor) on the cultured rat aortic vascular smooth muscle cells. METHODS: The plasmid contained the cDNA of AT_2 receptor was transfected into cultured rat vascular smooth muscle cells. The effects of AngⅡ, Ang Ⅱ+losartan, Ang Ⅱ+PD123319 on the expression of PCNA, the NOS activity and the cell number were observed. RESULTS: The cell number and the expression of PCNA decreased after the cells were treated with losartan. When treated with PD123319, the cell number and the expression of PCNA increased, but the expression of NOS decreased. CONCLUSIONS: These data suggest that when being activated, AT_2 receptor inhibits the proliferation of vascular smooth muscle cells and antagonizes the effect of AT_1 receptor, such an effect may be related to the activation of NOS. [
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Changes in lipids, enzymes and free-radical system of myocardial membranes were investigated in isoproterenol-induced myocardial infarction so as to study the modulative effects of Svate on myocardial membrane injury. Animals were killed 24h after ISP(85mg/kg) injection. The results suggested that disturbances in lipids metabolism, enzymes and free-radical system in ischemic myocardium, indicating the existence of myocardial membrane injury. In the Svate(0.25U/kg)-treated group, a beneficial effect of Svate exerted on membrane injury, as indicated by increased activities of GSH-Px, SOD and Na~+K~+-ATPase, and decreased Ch/PL ratio, MDA contents and Ca~(2+)-Mg~(2+)-ATPase activities.
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The kinetic alterations of plasma prekallikrcin(PKA) and antithrombin Ⅲ (AT-Ⅲ) following myocardial infarction induced by 2 injections subcutaneously of 85 mg isoproterenol/kg at 24 hours interval in rats were detected in this study, and the relationship between PKA, AT-Ⅲ and myocardial ischemia induced by isoproterenol were also discussed. It was found that the activity of PKA decreased significantly and AT-Ⅲ tended to decrease at 4 hours after the first injection of isoproterenol, both of the PKA and AT-Ⅲ at 24 hours were lower than those at 4 hours and evidently lower than those of normal control, and at 48 hours after the first injection of isoproterneol the PKA was still maintained at the same level of 24 hours but the AT-Ⅲ almost returned to the normal level.