氨基胍对去卵巢大鼠主动脉晚期糖化终末产物及血脂的影响

将 6月龄雌性SD大鼠随机分为假手术组 (sham)、去卵巢组 (OVX)和去卵巢 +氨基胍组 (OVX +AG)。去除双侧卵巢 2周后用氨基胍治疗 13周。禁食 2 4h ,放血处死动物 ,取血和主动脉 ,分别测定主动脉AGEs、血脂和血清过氧化物含量。结果表明 ,与假手术组比较 ,去卵巢组主动脉AGEs、甘油三脂 (TG)、氧化低密度脂蛋白 (OX LDL)、丙二醛 (MDA)均明显升高 (分别为P <0 0 1,P <0 0 5 ,P <0 0 5和P <0 0 1) ;高密度脂蛋白 胆固醇 (HDL C)、载脂蛋白AⅠ (apo AⅠ )和超氧化物歧化酶 (SOD)活性均显著降低 (均P <0 0 1)。氨基胍组与病理组比较 ,主动脉AGEs、血清TG、MDA和OX LDL均明显降低 (分别为P <0 0 1,P <0 0 5、P <0 0 5和P <0 0 1) ;HDL C、apo AⅠ和SOD活性均显著升高 (均P <0 0 1)。提示氨基胍通过降低去卵巢大鼠主动脉AGEs含量 ,降低大鼠血清OX LDL和TG水平 ,升高HDL C、apo AⅠ水平和SOD活性 ,发挥其对心血管的保护作用     

银杏叶及葡萄籽提取物体外抑制蛋白糖化终末产物生成作用的研究

 目的 应用体外蛋白糖化反应系统,确定银杏叶及葡萄籽提取物抑制蛋白糖化终末产物生成的作用。方法 对照组将葡萄糖与牛血清白蛋白分别在STUOX；条件下共同孵育，实验组则加入不同剂量的银杏叶及葡萄籽提取物或氨基胍。利用荧光分光光度计对不同温度和时间培养条件下的样品测定，根据荧光强度确定蛋白糖化终末产物的生成量。结果 在本体外系统中，蛋白糖化终末产物的生成与孵育温度及时间呈正相关。银杏叶提取物及葡萄籽提取物在1.0~2.0 g.L_-1剂量范围内均可有效抑制蛋白糖化终末产物的生成，当药物浓度达2.0 g·L_-1时其抑制作用相当于同剂量的氨基胍。结论 具有明确 抗氧化作用的银杏叶提取物及葡萄籽提取物在体外可有效抑制蛋白糖化终末产物的生成。     

降糖起萎合剂对糖尿病微血管病变大鼠阴茎海绵体糖基化终产物含量的影响

目的探讨降糖起萎合剂对糖尿病微血管并发症大鼠阴茎海绵体沉积的糖基化终产物(AGEs)的抑制作用.方法根据AGEs具有产生荧光的特点,通过测定其荧光强度,间接表示阴茎海绵体内AGEs的含量.结果及结论降糖起萎合剂对糖尿病微血管并发症大鼠阴茎海绵体沉积的荧光AGEs有较强的抑制作用.     

Antimicrobial activity in medicinal plants of the Scrophulariaceae and Acanthaceae

One hundred and one crude extracts obtained from various plant parts of 59 species representing mostly the plant families Scrophulariaceae and Acanthaceae have been investigated for their antimicrobial activity. Plants were selected using ethnobotanical and chemotaxonomic information. Growth inhibition using agar disk diffusion assays was determined against Escherichia coli, Pseudomonas aeruginosa, Staphylococcus aureus, and Candida albicans. Growth inhibitory activity against one or more of the microbial species was detected in over 40% of the samples.     

Serum levels of soluble form of receptor for advanced glycation end products (sRAGE) are positively associated with circulating AGEs and soluble form of VCAM-1 in patients with type 2 diabetes

We have recently found that soluble form of receptor for advanced glycation end products (sRAGE) levels are positively associated with inflammatory biomarkers and the presence of coronary artery disease (CAD) in type 2 diabetic patients. Since advanced glycation end products (AGEs) up-regulate RAGE expression and endogenous sRAGE could be generated from the cleavage of cell surface RAGE, it is conceivable that sRAGE is positively associated with circulating AGEs levels in diabetes. In this study, we examined whether sRAGE were correlated to circulating levels of AGEs and soluble forms of vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (sICAM-1) in patients with type 2 diabetes. Eighty-two Japanese type 2 diabetic patients underwent a complete history and physical examination, determination of blood chemistries, sRAGE, AGEs, sVCAM-1 and sICAM-1. Multiple regression analysis revealed that serum levels of AGEs and sVCAM-1 were independently correlated with sRAGE. This study demonstrated that serum levels of sRAGE were positively associated with circulating AGEs and sVCAM-1 levels in type 2 diabetic patients. Our present observations suggest sRAGE level may be elevated in response to circulating AGEs, thus being a novel marker of vascular injury in patients with type 2 diabetes.     

酶联免疫吸附分析方法(ELISA)检测血浆中糖基化终极产物

目的建立竞争性ELISA方法，测定血液中的高级糖化终产物的含量。方法对兔及牛血浆白蛋白进行体外葡萄糖修饰，得到糖基化终极产物抗原；用兔此抗原免疫新西兰大白兔得到与其特异结合的抗体。结果1．经过TNBS方法及聚丙稀凝胶电泳鉴定修饰抗原，发现修饰前后蛋白携带自由氨基数至少35％已被葡萄糖修饰且分子量也发生变化。2．免疫获得抗糖基化终极产物的多克隆抗体，并鉴定了此多抗只抗葡萄糖修饰的蛋白而不抗载体蛋白。3．用葡萄糖修饰的蛋白及其多克隆抗体制成ELISA试剂盒，批间、批内变异系数分别为5．8％和9．8％，灵敏度为0．5u／ml。结论得到检测血浆糖基化终极产物的ELISA试剂盒。     

Paeoniflorin protects HUVECs from AGE-BSA-induced injury via an autophagic pathway by acting on the RAGE

The aim of our study was to investigate the protective effects of Paeoniflorin (PF) against injury induced by AGE-modified bovine serum albumin (AGE-BSA) in human umbilical vein endothelial cells (HUVECs), and to examine the underlying mechanisms of these effects. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to determine cell viability. Protein expression levels were determined by western blotting. For function-blocking experiments, we used small interfering RNA molecules (siRNA) for function-blocking experiments. At 6 h, we found that 100 μg/mL AGE-BSA reduced the viability of HUVECs. However, pretreatment with PF restored cell viability in a dose-dependent manner. AGE-BSA increased the levels of microtubule-associated protein light chain 3-II (LC3-II) and the receptor for advanced glycation end products (RAGE). Expression of p62 protein was also increased, but not at a statistically significant level. Pretreatment with PF further increased levels of LC3-II and RAGE, but reduced the expression of p62. In cells transfected with Atg5 and RAGE siRNA, cell viability and expression of LC3-II decreased in both the AGE-BSA and PF + AGE-BSA treatments. PF can protect HUVECs from AGE-BSA-induced injury by upregulating autophagy and promoting the completion of autophagy flux. RAGE plays an important role in this autophagic protection effect.     

Role of CD11b+Gr-1+ myeloid cells in AGEs-induced myocardial injury in a mice model of acute myocardial infarction

Aims: Polymorph neutrophils are the predominant inflammatory cells and play a crucial role on the pathogenesis of myocardial injury at the early stage of acute myocardial infarction (AMI). However, the precursors and the differentiation of neutrophils are not fully understood. Here we explored the role of CD11b⁺Gr-1⁺ myeloid-derived suppressor cells (MDSCs) on myocardial injury in the absence and presence of advanced glycation end-products (AGEs) in a mice model of AMI. Methods and Results: Male C57BL/6J mice were selected. Fluorescent actived cell sortor (FACS) data demonstrated significantly increased CD11b⁺Gr-1⁺ MDSCs both in peripheral blood circulation and in the ischemic myocardium at 24 hours post AMI. Quantitative-real-time PCR results also revealed significantly upregulated CD11b and Ly6G mRNA expression in the ischemic myocardium. AGEs treatment further aggravated these changes in AMI mice but not in sham mice. Moreover, AGEs treatment also significantly increased infarction size and enhanced cardiomyocyte apoptosis. The mRNA expression of pro-inflammatory cytokine IL-6 and iNOS2 was also significantly increased in AMI + AGEs group compared to AMI group. Conclusion: These data suggest enhanced infiltration of MDSCs by AGEs contributes to aggravated myocardial injury in AMI mice, which might be one of the mechanisms responsible for severer myocardial injury in AMI patients complicating diabetes.     

玉葵清对糖基化终产物诱导的人肾系膜细胞趋化因子表达的影响

目的 探讨玉葵清对糖基化终产物（AGEs）诱导的人肾系膜细胞（HRMC）趋化因子表达及其趋化效应的影响. 方法 糖基化牛血清白蛋白（AGE-BSA）和玉葵清干预HRMC. 结果 AGE-BSA组较BSA组HRMC趋化单核细胞数增加,单核细胞趋化蛋白-1（MCP-1）、Fractalkine（FKN）中和抗体组HRMC趋化单核细胞数较AGE-BSA组减少;玉葵清组MCP-1、Fractalkine基因表达、上清中的蛋白含量和趋化单核细胞较BSA组降低（P＜0.05）. 结论 玉葵清减弱AGE-BSA诱导的HRMC趋化因子表达及其趋化效应,可能改善DN肾脏炎症反应.