大叶紫薇叶中降血糖活性成分的筛选

为筛选大叶紫薇叶中具有降血糖活性的成分,采用3T3-L1细胞葡萄糖消耗模型作为检测手段,对大叶紫薇叶提取物采用HP-20树脂吸附、溶剂萃取、制备薄层分离和制备高效液相分离,导向筛选具有降血糖作用的各分离组分.结果发现,大叶紫薇叶中corosolic acid、熊果酸和总三萜具有降血糖活性.     

模拟腰椎前路、后路间盘摘除术T12-L5腰段脊柱应力松弛蠕变实验研究

研究了18例新鲜尸体T12－L5腰段脊柱应力松弛，蠕变特性。测定了完整脊柱（正常组）及模拟前路（对照1组），后路手术（对照2组）腰段脊柱的应力松弛和蠕变效应，得出了在恒应变，应力条件下应力－时间曲线及数据，用回归分析的方法处理实验数据，得出了归一化应务松弛，蠕变函数及曲线，对前路间盘摘除术与后路间盘摘除术对脊柱粘弹性的影响进行分析讨论。     

Bisphenol a accelerates terminal differentiation of 3T3-L1 cells into adipocytes through the phosphatidylinositol 3-kinase pathway.

In order to identify whether bisphenol A (BPA) acts as an adipogenic agent, following the hormonal induction of differentiation into adipocytes, 3T3-L1 cells were treated for six days with BPA alone. Treatment with BPA increased the triacylglycerol (TG) content of the cultures, increased the percentage of Oil Red O-staining cells in the cultures, and increased the levels of lipoprotein lipase (LPL) and adipocyte-specific fatty acid binding protein (aP2) mRNAs. These findings indicate that BPA was able to accelerate terminal differentiation of 3T3-L1 cells into adipocytes. LY294002, a chemical inhibitor of phosphatidylinositol 3-kinase (PI 3-kinase), blocked completely the increasing effect of BPA on TG accumulation and expression of LPL and aP2 mRNAs. Western blot analysis revealed that BPA increased the level of phosphorylated Akt kinase. Based on these findings, we concluded that BPA acted through the PI 3-kinase and Akt kinase pathway, resulting in increased TG accumulation and expression of adipocyte genes. The structure-activity relationship for BPA-related chemicals was examined. Eight derivatives of BPA (three diphenylalkanes with different substituents at the central carbon atom, three diphenylalkanes with ester bonds on hydroxyl groups in the phenolic rings, one bisphenol consisting of a sulphur atom at the central position, one chemical with cyanic groups, instead of hydroxyl groups, in the phenolic rings) accelerated terminal adipocyte differentiation and their potencies to increase TG accumulation were 73-97% of that of BPA. Two diphenylalkanes with ether bonds on hydroxyl groups and two alkylphenols (4-nonylphenol and 4-tert-octylphenol) did not have the ability to accelerate terminal adipocyte differentiation.     

Anti-obesity effects of seaweeds of Jeju Island on the differentiation of 3T3-L1 preadipocytes and obese mice fed a high-fat diet

The seaweeds were collected from the coast of Jeju Island, South Korea. We investigated ethanol extracts from seaweed as potential antiobesity agents by testing their effect on adipogenic differentiation in 3T3-L1 cells. Among the red algae extracts tested, the Plocamium telfairiae extract (PTE) showed the highest inhibitory effect on lipogenesis in adipocytes and, thus, was selected as a potential antiobesity agent. PTE treatment significantly decreased the expression of the adipogenic-specific proteins peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein-α, sterol regulatory element-binding protein 1, and fatty acid-binding protein 4 compared with that in the untreated 3T3-L1 cells. PTE also inhibited high-fat diet (HFD)-induced obesity in male C57BL/6 mice. Oral administration of PTE significantly reduced the body weight, fatty liver, amount of white adipose tissue, and levels of triglyceride and glucose in the tested animals. Taken together, these data demonstrate that PTE can be developed as a therapeutic agent for obesity.     

Differential Immunohistochemical Expression of Syndecan-1 and Tumor Necrosis Factor Alpha in Colonic Mucosa of Patients with Crohn’s Disease

Tumor necrosis factor alpha (TNFα) in intestinal mucosa plays a key role in the inflammation characterizing Crohn’s disease (CD). Moreover, adhesion molecule syndecan-1 mediates the maintenance of mucosal integrity and supports tissue repair. Therefore, our aim in this study was to correlate simultaneous expression of TNFα and syndecan-1 in patients affected by CD. Biopsies from 10 patients with CD of large bowel and 10 subjects with irritable bowel syndrome (controls) were studied by immunohistochemical detection of both TNFα and syndecan-1 on successive serial sections. Overall labeling index (OLI) was indicated by the percentage of positive stromal (i.e., nonepithelial) cells/1000 counted in randomized fields, whereas selected labeling index (SLI) was represented by the simultaneous evaluation of both molecules in a same single selected field of each specimen. TNFα and syndecan-1 OLI were significantly higher in CD compared with controls, while SLI showed an inverse relationship between the molecules in CD which was not observed in controls. Epithelial syndecan-1 cytoplasmatic staining of superficial epithelium was associated with loss of basolateral staining in the crypts and high stromal TNFα in CD. In conclusion, TNFα and syndecan-1 expression is increased in the intestinal mucosa of patients with CD. However, the expression of the two molecules is inversely related when a single field is considered, these data supporting the possibility of a downregulation exerted by TNFα.     

Insulin stimulates IGFBP-2 expression in 3T3-L1 adipocytes through the PI3K/mTOR pathway

Insulin-like growth factor binding protein 2 (IGFBP-2) has been implicated in the etiology of several diseases, including the metabolic syndrome. Although IGFBP-2 derives mostly from the liver, recent evidence in mice and humans indicate that aging and obesity are associated with altered IGFBP-2 levels in white adipocytes. The present study was aimed at determining the mechanisms that control IGFBP-2 expression in mature adipocytes. IGFBP-2 mRNA and protein expression in serum-deprived 3T3-L1 adipocytes were twofold increased by acute insulin treatment. Co-treatments with the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin or the mammalian target of rapamycin (mTOR) inhibitor rapamycin blunted the effects of insulin. Coherently, IGFBP-2 mRNA levels were robustly increased in adipocytes lacking either TSC2 or 4E-BP1. Insulin triggered the recruitment of CAAT/enhancer binding protein α (C/EBPα) to the IGFBP-2 proximal promoter. These findings suggest that insulin upregulates IGFBP-2 expression through a PI3K/mTOR/C/EBPα pathway in white adipocytes.     

Fas凋亡相关基因在双酚A诱导成年雄性大鼠生殖毒性中的作用

目的探讨Fas凋亡途径相关基因在双酚A（BPA）诱导成年雄性大鼠生殖毒性中的作用。方法 40只成年Wistar雄性大鼠随机等分为4组：溶媒对照组（玉米油）和低、中、高剂量BPA喂养组（10、50、250μg/kg·bw/d）。大鼠在喂养35周后处死,称量睾丸、附睾、肝、肾及心脏重量并计算脏器系数;观察精子形态及计算精子畸形率。采用荧光实时定量PCR（RT-PCR）测定睾丸组织中自杀相关因子（Fas/Fas-L）、天冬氨酸特异酶切的半胱氨酸蛋白酶3（Caspase-3）mRNA含量。结果高剂量BPA喂养大鼠精子畸形率以及睾丸组织中Fas-L mRNA及Caspase-3 mRNA含量高于对照组,差异均有显著性（P!0.05）。结论在BPA的人体每日容许摄入量水平下（TDI=50μg/kg·bw/d）,未观察到生殖细胞损伤的效应;但长期经膳食暴露高剂量BPA（250μg/kg·bw/d）可致成年雄性大鼠生殖细胞损伤,其机制可能与BPA上调Fas-L mRNA和Caspase-3的表达有关。     

性激素对3T3-L1前脂肪细胞和脂肪细胞胰岛素敏感性的影响

目的观察不同浓度雌、雄激素对3T3-L1前脂肪细胞葡萄糖转运的影响,探讨性激素在胰岛素抵抗形成中的意义。方法体外培养3T3-L1前脂肪细胞,并诱导其分化成熟,利用2-脱氧-[3H]-D-葡萄糖掺入法,研究不同浓度的17β雌二醇、睾酮对胰岛素刺激的前脂肪细胞和脂肪细胞葡萄糖摄取能力的影响。结果10-8mol/L的17β雌二醇即能够抑制3T3-L1前脂肪细胞胰岛素刺激状态下的葡萄糖转运,且呈现明显的浓度依赖性抑制;而睾酮为10-8mol/L时3T3-L1前脂肪细胞胰岛素刺激状态下的葡萄糖转运并无明显影响,在浓度达到10-7mol/L开始出现抑制效应,浓度越高抑制效应越明显。结论性激素可以调节3T3-L1前脂肪细胞的胰岛素敏感性。