ABSTRACT
[Objective]To investigate the molecular mechanism of abnormal platelet activation induced by platelet O2 ·- and H2O2 levels in type 2 diabetes mellitus.[Methods]The platelet parameters in patients with type 2 diabetic patients and normal controls were measured;Immunofluorescence technique was used to observe the platelet morphology changing;Flow cytometry was used to detect platelet intracellular O2 ·- and H2O2 content in two groups,then with platelets in normal controls treated with NADH/PMS system and H2O2 respectively,platelet activation positive percentage was observed. Standard Western blot analysis protocols were used to detect expression difference of Catalase and type 2 super-oxide dismutase(Mn-SOD)in platelets.[Results]The MPV in the group of type 2 diabetic patients was significantly higher than in the normal control group(P < 0.001),but there was no statisticdifference in PLT,PDW,PCT between two groups. Immunofluorescence results showed that morphology of platelets in type 2 diabetic patients changed contrast to normal group. Through flowcytometry detection,the content of mitochondrial O2·-and H2O2 of platelet in type 2 diabetic patients were obviously higher than in normal group(P<0.05),whereas no significant difference in cytoplasmic O2·-. We adopted NADH/PMS system and H2O2 to treat platelets of normal group,heightened activated positive percentage were observed which described O2 ·- and H2O2 can significantly promote platelet activation(P<0.01). Western blot results showed that expression of Catalase in platelet of type 2diabetes patients decreased,while the expression and activity of Mn-SOD had no difference.[Conclusion]It is diabetic platelet Catalase expression decreased that may lead to Diabetic platelet mitochondrial O 2 ·- and H2O2 level increased ,thus regulating aberrant activation of diabetic platelet.
ABSTRACT
AIM: To investigate the effect of 188Re labeled monoclonal antibody on prostatic specific membrane antigen 7E11C5.3,radioimmunotherapy for the treatment of human prostate cancer cell line LNCaP in vitro.METHODS: 188Re-7E11C5.3 was prepared by direct 2-mercaptoethanol reduction method.Labeling efficiency and radiochemical purity was measured by paper chromatography.Immunoreactive fraction was determined by linear extrapolation.Cytotoxicity to LNCaP cells was determined by MTT assay.RESULTS: The labeling yield of 188Re-7E11C5.3 was(93.16?2.18)%,the radiochemical purity was(95.62?0.48)%,and the immunoreactive fraction was(74.86?1.86)%.The inhibitory effect of 188Re-7E11C5.3 on cell proliferation of LNCaP cells was significantly higher than that of 188Re-mIgG or 188ReO-4.The 50% inhibitory doses(IC50) of 188Re-7E11C5.3,188Re-mIgG,and 188ReO-4 were(23.38?3.73)?107 Bq/L,(59.21?8.02)?107 Bq/L and(68.89?10.91)?107 Bq/L,respectively.CONCLUSION: 188Re-7E11C5.3 can effectively inhibit the growth of in vitro cultured prostate cancer cells and shows much potential for prostate cancer radioimmunotherapy.
ABSTRACT
Objective: To study the effect of the bolus propofol on myocardial ? adrenergic receptor. Method: Twenty-one,aging 4-6 weeks,male health SD rats,were divided randomly into three groups:low dose group (L)with propofol of 5mg/kg,high dose group(H)with 12mg/kg of propofol and control group(C) with NS alone. The drugs were administered through the rat's tail vein in conscious state. 3 minutes after administration,the raps heart were totally taken out to investigate rat's myocardial ? adrenergic receptors with radioligand binding assay. Result:Compared with those in control group,in L group there was a decrease in ? adrenergic receptor density(Bmax),but no change in the affinity of ? adrenergic receptor (KD); In H group,Bmax decreased,KD value increased. The Bmax and KD were significantly different between L and H group. Conclusion:Intravenous bolus doses of propofol may cause down-regulation on myocardial ? adrenergic receptor of rats in dose-related way.