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Objective To study the role of natural antiox-LDL subclass IgM antibodies in formation of atherclerosis.Methods The macrophages from mice were divded into LDL group,Cuox-LDL group and control group.The macrophages in LDL group and Cuox-LDL group were precultured with LDL and Cuox-LDL.Adhesion experiment was performed in control group.3A6,5G8 and 2H7 were incubated.The macrophages were divided into 3A6 group,5G8 group and 2H7 group.Adhesion experiment was performed by adding the pretreated 125I Cuox-LDL.The binding parameters of macrophages and 125I Cuox-LDL in different groups were recorded.Foam cells were analyzed by cell lipid analysis with oil red O staining.Results The bound 125I Cuox-LDL level was significantly lower in Cuox-LDL group than in control group and LDL group (P＜0.01).No significant difference was found in bound 125I Cuox-LDL level between 5G3 group and 2H7 group (P＞0.05).The bound 125I Cuox-LDL level was significantly lower in 3A6 group than in control group,5G8 group and 2H7 group (P＜0.01).Oil red O staining showed no oil drop in macrophages,but a small number of oil drops in 3A6 group and a large number of oil drops in control group.The cholesterol and TG in macrophages reduced 45％ and the TG reduced 170％ in 3A6 group,which were significantly lower than those in control group (P＜0.01).Conclusion Antiox-LDL IgM subclass antibody 3A6 can effectively prevent the binding of unactivated macrophages to ox-LDL,reduce the occurrence and progression of atherosclerosis.
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Objective To investigate the sustained release of BSA from chitosan-OREC/BSA films coated mats in vitro.Methods The negatively charged cellulose acetate (CA) fibrous mats were modified with multilayers of the positively charged chitosan or chitosan-OREC intercalated composites and the negatively charged bovine serum albumin (BSA) via electrostatic layer-by-layer (LBL) self-assembly technique.The adsorption and rinsing steps were repeated until the desired number of deposition bilayers was obtained.The in vitro BSA encapsulation and release experiments demonstrated that OREC could affect the degree of protein loading capacity and release ficiency of the LBL films coating.Results In the pH-gradient release assay,only a small amount of BSA was released from the mats in 1 h.As the time increased,the release rate of BSA of all the samples gradually went up to the maximum data within 8 h.For the samples with identical number of bilayers and record time,obvious increasing of the release amount could be seen in pH 7.4,in comparison with pH 1.2.Besides,doubling bilayers film-coated mats generally.Meanwhile,it was slightly distinguishable between 5 and 5.5 as well as 10 and 10.5 bilayers (t=0.651～ 1.324,P＞0.05).Interestingly,it could be seen that protein release of the chitosan-OREC/BSA films coated mats remarkably increased compared with that of chitosan/BSA films coated mats(t=2.264～ 2.305,P＜0.05).Conclusion The release of protein in the initial time could be controlled by adjusting the number of deposition bilayers,the outmost layer and the composition of coating bilayers.
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Objective To explore the role and the possible molecular mechanisms of natural anti-oxLDL IgM monoclonal antibody played and involved in pathogenesis of atherosclerosis. Methods Natural anti-oxLDL IgM monoclonal antibody 3A6 was generated by using standard hybridoma production techniques. Influence of 3A6 on formation of foam cells was observed by Oil Red O staining and affinity of Na125I-conjugated oxLDL on the naive and LPS-activated macrophages. After LPS stimulation on macrophages, anti-TLR4 neutralizing mAb, p38MAPK specific inhibitor SB203580, NF-kB specific inhibitor PDTC or RNAi targeting Fcα/μ receptor (Fcamr) were applied, respectively. Results Natural anti-oxLDL IgM monoclonal antibody 3 A6 were found specifically inhibit the binding of CuoxLDL to naive macrophages but not the binding of CuoxLDL to LPS-activated macrophages. It also promoted the formation of CuoxLDL-mediated foam macrophages. 3A6 F(ab')2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. LPS up-regulated the expression of Fcamr in macrophages in a dose- and time-dependent manner, which was attenuated by treatment with anti-TLR4. LPS induced the phosphorylation of p38MAPK and translocation of NF-kB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages. Conclusions Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to naive macrophages in vitro. However, LPS, through the Toll-like receptor (TLR)4 receptor, activated the p38MAPK and NF-kB pathways and up-regulated the expression of Fcα/μ receptor in macrophages, which promoted the binding of 3A6/CuoxLDL complex to macrophages through binding with Fc fragments and the formation of foam macrophages. Therefore, our findings provide a new explanation why bacterial infection deteriorates the pathogenesis of atherosclerosis.
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Objective:To evaluate the effects of low dosage sufentanil used for blind nasotracheal intubation.Methods:Sixty cases for maxillofacial surgery were divided into 3 groups randomly with 20 in each group. Patients in groupⅠwere administered with fentanyl and midazolam by vein, those in groupⅡ with fentanyl and droperidol by vein,those in group Ⅲ with sufentanil at 0.1~0.2 ?g/kg. Intramuscular premedication of atropine-midazolam and blind nasotracheal intubation were performed in all cases after surface anesthesia for routine. Blood pressure(BP), heart rate (HR), mean artery pressure (MAP), blood oxygen saturation of pulse (SpO_2), intubation complication(IC), intubation achievement ratio(IAR), sedation score (Ramsay score), patient satisfaction(PS), and the incident rate of amnesia(IRA) in the three groups at T1 (before administering drug), T2 (after administering drug) and T3 (when tracheal tube was inserted into tracheal) were measured and observed. Results:In groups I and Ⅱ Ramsay score increased to 3～5, MAP and SpO_2 decreased (P0.05).Conclution:The low dose sufentanil can be applied for the sedation and analgesic before blind nasotracheal intubation.
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Objective To study effects of constant magnetic fields(CMF) on the intracellular free calcium of human umbilical arterial vascular smooth muscle cells to discuss the mechanism of CMF affecting the proliferation of VSMC.Methods The intracellular free calcium concentration of human umbilical arterial vascular smooth muscle cells was detected by laser scanning confocal microsopy.Results The CMF affected the intracellular free calcium concentration of human umbilical arterial vascular smooth muscle cells.The CMF(5 mT) caused a persistent decrease of intracellular free calcium concentration of VSMC from 10 min to 50 min.Conclusion The CMF could inhibit proliferation of VSMC by decreasing the intracellular free calcium constant magnetic field concentration of VSMC.The CMF could markedly inhibit proliferation of VSMC,which might be useful in treatment of RS after PTCA.