CLA对急性缺氧大鼠肝脏线粒体呼吸链酶活性及氧化应激的影响

目的:观察共轭亚油酸(CLA)对急性缺氧大鼠肝脏线粒体呼吸链酶活性及肝脏内氧化应激(OS)的影响。方法:将60只SD大鼠随机分为正常对照组,模拟海拔5000米高原环境连续缺氧暴露3d的急性缺氧组,急性缺氧CLA干预组。生化法测定肝脏组织中丙二醛(MDA)、还原型谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性,Clark氧电极法观察大鼠肝脏线粒体呼吸链酶活性。结果:成功诱导大鼠急性缺氧模型。与对照组比,急性缺氧组大鼠肝脏MDA含量明显升高(P<0.05),同时肝脏线粒体呼吸链酶活性以及抗氧化酶活性(SOD,CAT)及GSH显著降低(P<0.05),与急性缺氧相比,CLA治疗组大鼠以上各项指标均有改善,并存在一定的剂量效应关系。结论:CLA通过抑制氧化应激增强大鼠肝脏线粒体呼吸链酶活性改善了急性缺氧大鼠肝脏的能量代谢障碍,对急性缺氧引起的氧化损伤有保护作用。     

Critical role of Toll‐like receptor 2 in Bacteroides fragilis‐mediated immune responses in murine peritoneal mesothelial cells

In this study, the role of Toll‐like receptor 2 (TLR2) in immune responses of murine peritoneal mesothelial cells against Bacteroides fragilis was investigated. Enzyme linked immunosorbent assay was used to measure cytokines and chemokines. Activation of nuclear factor κB (NF‐κB‐α) and mitogen‐activated protein kinases (MAP kinases) was investigated by western blot analysis. B. fragilis induced production of interleukin‐6, chemokine (C‐X‐C motif) ligand 1 (CXCL1) and chemokine (C‐C motif) ligand 2 (CCL2) in wild type peritoneal mesothelial cells; this was impaired in TLR2‐deficient cells. In addition, in response to B. fragilis, phosphorylation of inhibitory NF‐κB‐α and c‐Jun N‐terminal kinase mitogen‐activated protein kinase (MAPK) was induced in wild type mesothelial cells, but not in TLR2‐deficient cells,. Inhibitor assay revealed that NF‐κB and MAPKs are essential for B. fragilis‐induced production of CXCL1 and CCL2 in mesothelial cells. These findings suggest that TLR2 mediates immune responses in peritoneal mesothelial cells in response to B. fragilis.     

MicroRNA-processing enzyme Dicer is required in epicardium for coronary vasculature development

The epicardium is a sheet of epithelial cells covering the heart during early cardiac development. In recent years, the epicardium has been identified as an important contributor to cardiovascular development, and epicardium-derived cells have the potential to differentiate into multiple cardiac cell lineages. Some epicardium-derived cells that undergo epithelial-to-mesenchymal transition and delaminate from the surface of the developing heart subsequently invade the myocardium and differentiate into vascular smooth muscle of the developing coronary vasculature. MicroRNAs (miRNAs) have been implicated broadly in tissue patterning and development, including in the heart, but a role in epicardium is unknown. To examine the role of miRNAs during epicardial development, we conditionally deleted the miRNA-processing enzyme Dicer in the proepicardium using Gata5-Cre mice. Epicardial Dicer mutant mice are born in expected Mendelian ratios but die immediately after birth with profound cardiac defects, including impaired coronary vessel development. We found that loss of Dicer leads to impaired epicardial epithelial-to-mesenchymal transition and a reduction in epicardial cell proliferation and differentiation into coronary smooth muscle cells. These results demonstrate a critical role for Dicer, and by implication miRNAs, in murine epicardial development.     

Peripheral Effects of Nesfatin-1 on Glucose Homeostasis

Aims/hypothesis

The actions of peripherally administered nesfatin-1 on glucose homeostasis remain controversial. The aim of this study was to characterize the mechanisms by which peripheral nesfatin-1 regulates glucose metabolism.

Methods

The effects of nesfatin-1 on glucose metabolism were examined in mice by continuous infusion of the peptide via osmotic pumps. Changes in AKT phosphorylation and Glut4 were investigated by Western blotting and immnuofluorescent staining. Primary myocytes, adipocytes and hepatocytes were isolated from male mice.

Results

Continuous peripheral infusion of nesfatin-1 altered glucose tolerance and insulin sensitivity in mice fed either normal or high fat diet, while central administration of nesfatin-1 demonstrated no effect. Nesfatin-1 increases insulin secretion in vivo, and in vitro in cultured min6 cells. In addition, nesfatin-1 up-regulates the phosphorylation of AKT in pancreas and min6 islet cells. In mice fed normal diet, peripheral nesfatin-1 significantly increased insulin-stimulated phosphorylation of AKT in skeletal muscle, adipose tissue and liver; similar effects were observed in skeletal muscle and adipose tissue in mice fed high fat diet. At basal conditions and after insulin stimulation, peripheral nesfatin-1 markedly increased GLUT4 membrane translocation in skeletal muscle and adipose tissue in mice fed either diet. In vitro studies showed that nesfatin-1 increased both basal and insulin-stimulated levels of AKT phosphorylation in cells derived from skeletal muscle, adipose tissue and liver.

Conclusions

Our studies demonstrate that nesfatin-1 alters glucose metabolism by mechanisms which increase insulin secretion and insulin sensitivity via altering AKT phosphorylation and GLUT 4 membrane translocation in the skeletal muscle, adipose tissue and liver.     

高等植物开花时程的基因调控(Ⅱ)

主要探讨如下几个问题:转基因植物中的拟南芥开花时程基因;拟南芥中的甲基化与实验胚胎学研究;高等植物开花时程控制的可能机制.目前本领域已成为植物发育分子生物学的前沿热点研究领域之一.结合有关工作,对这一世界性热门领域进行了系统的评述,希望能为国内同行提供有关参考,赶超世界的植物分子生物学先进水平,对分子水平与生物技术角度改良黄土高原生态环境有指导意义.     

高效液相色谱法制备Ⅰ型胶原蛋白及其性质研究

从猪皮中分离纯化I型胶原蛋白,并对其部分性质进行研究。采用粗提法,高效液相色谱半制备法进行分离纯化,用分析型高效液相色谱检测纯度,同时对其理化性质进行鉴定,并对所提取的胶原进行全身急性毒性试验及皮肤致敏试验。高效液相色谱测定结果显示所得样品为一单峰,理化性质测定结果符合I型胶原蛋白特征;通过整体水平的安全性评价,表明该方法提取的I型胶原蛋白具有较大的安全性和可靠性。因此,用高效液相色谱可制得高纯度且具有良好生物安全性的I型胶原蛋白。     

拟衣藻系统分类新证据

拟衣藻 (Chloromonas)与衣藻属 (Chlamydomonas)的亲缘关系及分类学位置在藻类学界一直没有定论。其重要原因是单细胞鞭毛类是否具有蛋白核这一特征在系统分类学上具有重要意义 ,而光镜形态与色素体上具 1到多个蛋白核的衣藻极其相似的拟衣藻 ,其不具蛋白核这一特征的稳定性受到许多学者的怀疑。本文观察并报道了中华拟衣藻 (ChloromonasSinica)的超微结构 ,通过对拟衣藻与衣藻超微结构的探究和比对 ,发现除了从孢子时期开始的整个生活史中 ,中华拟衣藻都不具蛋白核外 ,无论显微还是超微结构 ,拟衣藻与衣藻都显示出高度的相似性。从而提出在尚未获得更多资料之前 ,将拟衣藻从衣藻属分离出来成为独立的属较为合适