Saccharide Polymers, 5

Summary: New “saccharide polymers” were synthesized via free radical polymerization. The saccharide compounds in copolymerisation reactions were 2,4,6‐tri‐O‐acetyl‐3‐deoxy‐D ‐erythro‐hex‐2‐enono‐1,5‐lactone ( 1 ), (Ac‐GEL 1 ) and 2,4,6‐tri‐O‐benzoyl‐3‐deoxy‐D ‐erythro‐hex‐2‐enono‐1,5‐lactone ( 2 ), (Bz‐GEL 2 ). These sugar monomers are easily obtained with high yield in a one step reaction from glucono‐δ‐lactone. They have a pyranoid structure containing an endocyclic double bond and they are electron acceptor compounds. Copolymerization reactions were carried out in solution and in substance. Copolymers with different sugar contents and low as well as high molecular weights were obtained. The structures and the compositions of the soluble saccharide polymers were established by elemental analysis, polarimetry, FTIR spectroscopy, ¹H and ¹³C NMR spectroscopy. Some characteristic properties, e.g., molecular weight, optical rotation and copolymerization parameters are reported.

Schematic conversion of glucono‐δ‐lactone to saccharide monomers.     

马桑内酯癫痫大鼠脑内ETmRNA表达的改变

目的：本文从分子水平观察马桑内酯所致的癫痫大鼠脑内ETmRNA表达以及硝苯吡啶对其表达的影响,进而分析ET在马桑内酯癫痫中的可能作用。方法：将24只SD大鼠分三组（生理盐水对照组、癫痫组和抗痫组）,采用自行标记的地高辛－ET RNA探针作大鼠脑片原位杂交。结果：在癫痫大鼠脑切片的广泛区域可见阳性杂交信号,尤以下丘脑和海马为明显;抗痫组（硝苯吡啶＋马桑内酯）大鼠脑内均未见到明显的杂交信号,与生理盐水对照组相似。表明马桑内酯致痫时,大鼠脑内ETmRNA表达增强,该作用可被L－型Ca^2 通道阻断剂硝苯吡啶阻断。结论：ET在马桑内酯致痫时,可能作为一种神经肽,通过激活L－型Ca^2 通道使细胞内Ca^2 浓度增加而产生致痫作用。     

海马损伤对大鼠学习能力的影响及与安定相关性研究

目的 :观察海马损伤大鼠癫痫发作和使用安定控制其发作程度的大鼠主动性条件回避反应的变化 ,从而判断其学习能力的改变。方法 :用肌注马桑内酯 (cariarialactone) ,建立海马cA1 区神经元坏死大鼠癫痫模型。部分大鼠肌注安定控制癫痫发作程度和次数 ,再检测主动性条件回避反应的正确习得率 (80 %为学会标准 )。结果 :海马损伤大鼠的学习能力降低。结论 :海马损伤癫痫发作大鼠的学习能力显著下降 ,安定对癫痫大鼠的学习能力具有显著的保护作用。     

没药化学成分及抗炎活性研究

目的 研究没药Myrrha二氯甲烷部位化学成分及部分化合物抗炎活性。方法 采用多种柱色谱方法和制备液相色谱进行分离纯化,并利用波谱学方法对其结构进行鉴定。通过检测化合物对脂多糖(lipopolysaccharide,LPS)诱导的BV2细胞释放炎症介质NO的抑制能力,来评估所分离化合物的抗炎作用。结果 从没药的二氯甲烷部位中分离得到15个化合物,通过波谱数据与文献数据进行对比,分别鉴定为苍术内酯Ⅲ(1)、myrrhterpenoid N(2)、木香烃内酯(3)、莪术二酮(4)、去氢假虎刺酮(5)、eurylosesquiterpenol E(6)、t-杜松醇(7)、10β-hydroxyisodauc-6-en-14-al(8)、oplopanone(9)、去氢木香内酯(10)、4-hydroxy-4,7-dimethyl-α-tetralone(11)、3-hydroxy-6-methylacetophenone(12)、(2E,4E)-6-hydroxy-2,6-dimethylhepta-2,4-dienal(13)、erlangerin D(14)、(-)-dimethylma...     

一测多评法同时测定蒙药古日古木-13丸中6种成分

目的建立古日古木-13丸中6种成分没食子酸、羟基红花黄色素A、栀子苷、鞣花酸、木香烃内酯、去氢木香内酯的一测多评方法,验证该方法在古日古木-13丸质量分析中应用的科学性与可行性。方法采用HPLC法,以栀子苷为内参物,建立没食子酸、羟基红花黄色素A、鞣花酸、木香烃内酯、去氢木香内酯的相对校正因子(fs/i),并利用fs/i计算古日古木-13样品中该5种成分的含量,同时采用外标法计算各成分的含量,并比较2种方法差异。结果没食子酸、羟基红花黄色素A、鞣花酸、木香烃内酯、去氢木香内酯的fs/i分别为0.481 0、0.906 4、0.170 9、0.971 2、1.261 5。一测多评法与外标法得到的6批古日古木-13丸样品含量测定结果 RSD<2.0%,没有显著差异。结论以栀子苷为内参物建立fs/i准确,易行,一测多评法可以用于古日古木-13丸中多指标成分的质量评价。     

蝎毒对马桑内酯所致癫（间）大鼠的作用

目的研究蝎毒素对癫（间）的作用,为新药的开发利用提供理论基础.方法采用整体马桑内酯大鼠癫（间）模型,侧脑室埋管给药,记录皮层脑电图.结果蝎毒素能延长马桑内酯所致癫（间）发作的潜伏期,降低发作程度,缩短发作时间.结论蝎毒素对马桑内酯所致的大鼠癫（间）具有对抗作用.     

利血平对马桑内酯致痫作用和癫痫小鼠脑内cAMP水平的影响

给White Chengdu number 1(WC_1)小鼠腹腔注射利血平1mg/kg,能明显降低其皮层和海马的cAMP水平,加重马桑内酯所致WC_1小鼠癫痫发作的程度,增加癫痫的发作率,减小引起发作的阈值剂量。利血平预处理动物还能明显抑制癫痫发作时皮层和海马cAMP的增加。这些结果提示,癫痫发作活动引起的某些脑区cAMP增加可能与单胺递质活性有关。     

Role of Ca2+-independent phospholipase A2 and cytochrome P-450 in store-operated calcium entry in 3T6 fibroblasts

Store-operated calcium (SOC) channels and capacitative Ca2+ entry play a key role in cellular functions, but their mechanism of activation remains unclear. Here, we show that thapsigargin induces [3H] arachidonic acid (AA) release, 45Ca2+ influx and a subsequent enhancement of intracellular calcium concentration ([Ca2+]i. Thapsigargin-induced elevation of [Ca2+]i was inhibited by cytochrome P-450 inhibitors and by cytochrome P-450 epoxygenase inhibitor and was reverted by 11,12 EET addition. However, cyclooxygenase and lipoxygenase inhibitors have no effect. Moreover, we observed that four EETs were able to induce 45Ca2+ influx. Finally, we reported that the effect of 11,12 EET on 45Ca2+ influx was sensible to receptor-operated Ca2+ channel blockers (NiCl2, LaCl3) but not to voltage-dependent Ca2+ channel blocker as verapamil. Thus, AA released by Ca2+-independent phospholipase A2 and AA metabolism through cytochrome P-450 pathway may be crucial molecular determinant in thapsigargin activation of SOC channels and store-operated Ca2+ entry pathway in 3T6 fibroblasts. Moreover, EETs, the main cytochrome P-450 epoxygenase metabolites of AA, are involved in thapsigargin-stimulated Ca2+ influx. In summary, our results suggest that EETs are components of calcium influx factor(s).     

High-molecular-weight polyethylene glycol prevents lethal sepsis due to intestinal Pseudomonas aeruginosa

BACKGROUND & AIMS: During stress, erosion of protective intestinal mucus occurs in association with adherence to and disruption of the intestinal epithelial barrier by invading opportunistic microbial pathogens. The aims of this study were to test the ability of a high-molecular-weight polyethylene glycol compound, polyethylene glycol 15-20, to protect the intestinal epithelium against microbial invasion during stress. METHODS: The ability of polyethylene glycol 15-20 to protect the intestinal epithelium against the opportunistic pathogen Pseudomonas aeruginosa was tested in cultured Caco-2 cells. Bacterial virulence gene expression, bacterial adherence, and transepithelial electrical resistance were examined in response to apical inoculation of P. aeruginosa onto Caco-2 cells. Complementary in vivo studies were performed in a murine model of lethal sepsis due to intestinal P. aeruginosa in which surgical stress (30% hepatectomy) was combined with direct inoculation of P. aeruginosa into the cecum. RESULTS: High-molecular-weight polyethylene glycol (polyethylene glycol 15-20) conferred complete protection against the barrier-dysregulating effects of P. aeruginosa in Caco-2 cells. Intestinal application of polyethylene glycol 15-20 in stressed mice protected against the lethal effects of intestinal P. aeruginosa. Mechanisms of this effect seem to involve the ability of polyethylene glycol 15-20 to distance P. aeruginosa from the intestinal epithelium and render it completely insensate to key environmental stimuli that activate its virulence. CONCLUSIONS: High-molecular-weight polyethylene glycol has the potential to function as a surrogate mucin within the intestinal tract of a stressed host by inhibiting key interactive events between colonizing microbes and their epithelial cell targets.