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101.
目的: 观察木瓜蛋白酶对单核细胞-血小板聚集物(MPA)诱导的单核细胞分泌和黏附功能的抑制作用,并初步探讨其分子机制。方法: 分离人外周血单核细胞和富血小板血浆(PRP),检测20 U/L木瓜蛋白酶不同作用方式下凝血酶和花生四烯酸(AA)诱导的MPA形成及肿瘤坏死因子-α(TNF-α)水平。将实验分为0(对照)、20、80 U/L木瓜蛋白酶组,分别以ELISA、流式细胞术和显微镜检查测定木瓜蛋白酶与单核细胞共孵育后MPA诱导的单核细胞趋化蛋白-1(MCP-1)和组织因子(TF)释放、CD11b和CC趋化因子受体2(CCR2)表达水平以及单核细胞与人脐静脉内皮细胞黏附率,再以Western blot检测单核细胞Akt磷酸化(p-Akt)和环氧化酶-2(COX-2)表达水平。结果: 20 U/L木瓜蛋白酶与单核细胞和血小板共孵育时显著降低凝血酶和AA诱导的MPA形成和TNF-α 水平(P<0.01)。20 U/L木瓜蛋白酶组MCP-1和TF水平,CD11b和CCR2表达率,单核细胞与内皮细胞黏附率均显著低于对照组(P<0.01),80 U/L组对五者的抑制率显著高于20 U/L组(P<0.01)。木瓜蛋白酶显著抑制p-AKT和COX-2表达,80 U/L组p-Akt和COX-2光密度比值显著低于20 U/L组(P<0.01)。结论:木瓜蛋白酶可通过抑制Akt磷酸化和COX-2表达途径而抑制MPA诱导单核细胞活化后的释放和黏附功能,从而可能有助于预防动脉粥样硬化。 相似文献
102.
Pregel Marko J.; Shen Shi-Hsiang; Storer Andrew C. 《Protein engineering, design & selection : PEDS》1995,8(12):1309-1316
The regulatory roles of the two src homology 2 (SH2) domainsof protein tyrosine phosphatase 1C were investigated by comparingrecombinant full-length PTP1C with mutants in which either theN-terminal SH2 (N-SH2) domain (PTP1CANSH2), the C-terminal SH2(C-SH2) domain (PTP1CACSH2) or both SH2 domains were deleted(PTP1CANSH2ACSH2). This revealed that the SH2 domains have opposingand independent effects on activity: strong inhibition by N-SH2(42-fold) and weak activation by C-SH2 (2.1-fold). C-SH2 causedactivation across a wide pH range while N-SH2 inhibited mostat neutral and high pH through a shift of the basic limb ofthe pH profile of kmt/Km, apparently via perturbation of anactive-site pKa value. A phosphotyrosyl peptide derived fromthe erythro-poietin receptor caused an {small tilde}30-foldactivation of PTP1C and PTP1CACSH2 but had no effect on PTP1CANSH2or PTP1CANSH2ACSH2, indicating that binding of this peptideto N-SH2 abolished its inhibition. Since C-SH2 separates N-SH2from the catalytic domain in full-length PTP1C and activationis observed for PTP1CACSH2, it appears that the inhibitory effectof N-SH2 is independent of the position in the sequence andthat intermolecular interactions may also be possible 相似文献
103.
Lanonol phosphate was synthesized by a sustained-release phosphorylation reaction method using P2O5 dispersed in lanonol phosphate. The phosphorylation reaction studies confirmed the best condition was a reaction temperature
of 75 °C, a reaction time of 2.5 h and a molar ratio of hydroxyl and P2O5 of 3.0:1.0. The mole fraction of monoalkyl phosphate made by the sustained-release method increased by 14.3% compared to that
obtained by the direct addition of P2O5. Preparation of lanonol phosphates by this method overcomes the agglomeration problem of phosphorus pentoxide, and the reaction
rate is steady. Since lanonol phosphate was used as the dispersant for P2O5 powder, impurities due to the presence of other dispersants were eliminated, allowing synthesis of a nearly pure product.
A mixture of monoalkyl phosphate and dialkyl phosphate with high monoalkyl content is obtained with light color. It is an
eco-friendly reaction with minimal waste.
相似文献
Qiang TaotaoEmail: |
104.
Kozikowski AP Gaisina IN Petukhov PA Sridhar J King LT Blond SY Duka T Rusnak M Sidhu A 《ChemMedChem》2006,1(2):256-266
Research by Klein and co-workers suggests that the inhibition of GSK-3beta by small molecules may offer an important strategy in the treatment of a number of central nervous system (CNS) disorders including Alzheimer's disease, Parkinson's disease, and bipolar disorders. Based on results from kinase-screening assays that identified a staurosporine analogue as a modest inhibitor of GSK-3beta, a series of 3-indolyl-4-indazolylmaleimides was prepared for study in both enzymatic and cell-based assays. Most strikingly, whereas we identified ligands having poor to high potency for GSK-3beta inhibition, only ligands with a Ki value of less than 8 nM, namely maleimides 18 and 22, were found to inhibit Tau phosphorylation at a GSK-3beta-specific site (Ser 396/404). Accordingly, maleimides 18 and 22 may protect neuronal cells against cell death by decreasing the level of alpha-Syn protein expression. We conclude that the GSK-3beta inhibitors described herein offer promise in defending cells against MPP+-induced neurotoxicity and that such compounds will be valuable to explore in animal models of Parkinson's disease as well as in other Tau-related neurodegenerative disease states. 相似文献
105.
106.
为提高壳聚糖支架材料的孔隙率及矿化程度,通过磷酸化表面改性和仿生矿化制备了磷酸化(PCSW)和生物矿化(BMCW)木垛型壳聚糖多孔支架.FTIR结果显示,壳聚糖分子中有磷酸根的引入.XRD结果表明,矿化24 h后支架上形成结晶度较高的磷酸钙盐晶体,矿化48 h后结晶度明显增加并形成单纯的羟基磷灰石(HA)结晶.SEM观察发现,在支架的内外表面均致密地沉积了HA晶体层.压缩强度测试结果表明,复合支架BMCW矿化48 h的压缩强度为(0.54±0.005) MPa,压缩模量为(5.47±0.65) MPa,BMCW可用作非承重骨组织修复材料. 相似文献
107.
为提高壳聚糖支架材料的孔隙率及矿化程度, 通过磷酸化表面改性和仿生矿化制备了磷酸化(PCSW)和生物矿化(BMCW)木垛型壳聚糖多孔支架。FTIR结果显示, 壳聚糖分子中有磷酸根的引入。XRD结果表明, 矿化24 h后支架上形成结晶度较高的磷酸钙盐晶体, 矿化48 h后结晶度明显增加并形成单纯的羟基磷灰石(HA)结晶。SEM观察发现, 在支架的内外表面均致密地沉积了HA晶体层。压缩强度测试结果表明, 复合支架BMCW矿化48 h的压缩强度为(0.54±0.005) MPa, 压缩模量为(5.47±0.65) MPa, BMCW可用作非承重骨组织修复材料。 相似文献
108.
109.
110.
Stress granules (SGs) and processing bodies (P bodies) are cytoplasmic domains and play a role in the control of translation and mRNA turnover in mammalian cells subjected to environmental stress. Recent studies have revealed that SGs also form in the budding yeast Saccharomyces cerevisiae in response to glucose depletion and robust heat shock. However, information about the types of stress that cause budding yeast SGs is quite limited. Here we demonstrate that severe ethanol stress generates budding yeast SGs in a manner independent of the phosphorylation of eIF2α. The concentration that generated budding yeast SGs (>10%) was higher than that causing P bodies (>6%), and P bodies were assembled prior to SGs. As well as mammalian SGs, the assembly of budding yeast SGs under ethanol stress was blocked by cycloheximide. On the other hand, the budding yeast SGs caused by ethanol stress contained eIF3c but not eIF3a and eIF3b, although the eIF3 complex is a core constituent of mammalian SGs. Moreover, null mutants (pbp1Δ, pub1Δ and tif4632Δ) with a strong reduction in SG formation did not resume proliferation after the elimination of ethanol stress, indicating that the formation of budding yeast SGs might play a role in sufficient recovery from ethanol stress. 相似文献