香茶菜属植物中的三萜化合物对脂质过氧化和DNA损伤的保护作用

通过检测对H2O2处理的人外周血单个核细胞的DNA损伤、鼠肝微粒体脂质过氧化和pBR322 DNA氧化断裂的保护作用,测定了从香茶菜中提取到的4种三萜化合物的抗氧化活性.结果表明,4种化合物在这3种体系中发挥着不同的作用.熊果酸在所有体系中保护作用最强;2α,3β-二羟基-乌苏-12-烯-28-酸在抑制脂质过氧化时活性强,而在抑制单链DNA断裂中作用较弱;其异构体2α,3α-二羟基-乌苏-12-烯-28-酸作用正好相反;齐墩果酸仅在在H2O2处理的单个核细胞层DNA损伤中具有微弱保护作用.     

Isoprenylation in regulation of signal transduction by G-protein-coupled receptor kinases.

Rhodopsin kinase and beta-adrenergic receptor kinase (beta ARK) are related members of a serine/threonine kinase family that specifically initiate deactivation of G-protein-coupled receptors. After stimulus-mediated receptor activation, these cytoplasmic kinases translocate to the plasma membrane. Here we show that the molecular basis for this event involves a class of unsaturated lipids called isoprenoids. Covalent modification in vivo of rhodopsin kinase by a 15-C (farnesyl) isoprenoid enables the kinase to anchor to photon-activated rhodopsin. Mutations that alter or eliminate the isoprenoid, fully disable light-specific Rhodopsin kinase translocation. Other receptor kinases (such as beta ARK), which lack an intrinsic lipid, are activated on exposure to brain beta gamma subunits of the signal-transducing G proteins, the gamma subunit of which bears a 20-C (geranylgeranyl) isoprenoid. Using chimaeric beta ARKs that undergo isoprenylation in vitro, we demonstrate that membrane association and activation of these kinases can occur in the absence of beta gamma. These results indicate that rhodopsin kinase (by means of an integral isoprenoid) and beta ARK (through its association with beta gamma) both rely on the function of isoprenyl moieties for their translocation and activity, illustrating distinct, though related, modes of biological regulation of receptor function.     

Molecular and genetic damage in humans from environmental pollution in Poland.

Extreme environmental pollution such as that found in the highly industrialized Silesian region of Poland has been associated with increased risk of cancer and adverse reproductive outcomes. Among the most prevalent carcinogenic and mutagenic air pollutants in Silesia are the polycyclic aromatic hydrocarbons (PAH) which are largely produced by industrial and residential combustion of coal. Molecular epidemiology aims to prevent disease by using biological markers to identify risks well before clinical onset to allow effective intervention. Here, we use a battery of biological markers to measure molecular and genetic damage in peripheral blood samples from residents of Silesia and from persons living in a rural, less polluted area of Poland. The results show that their exposure to environmental pollution is associated with significant increases in carcinogen-DNA adducts (PAH-DNA and aromatic adducts), in sister chromatid exchange including high-frequency cells, and in chromosomal aberrations as well as a doubling in the frequency of ras oncogene overexpression. We found that aromatic adducts on DNA were significantly correlated with chromosomal mutation, providing us with a molecular link between environmental exposure and a genetic alteration relevant to cancer and reproductive risk.     

高校图书馆在非物质文化遗产保护中的角色定位与实践

阐述了非物质文化遗产保护的意义和高校图书馆对参与非物质文化遗产抢救保护的优势,论述了高校图书馆在非物质文化遗产保护中的角色定位.参与非物质文化遗产保护,高校图书馆的功能可以拓展、延伸.结合实践探讨了高校图书馆参与非物质文化遗产收集、整理、传递的内容与方式.     

高校图书馆在非物质文化遗产保护中的角色定位与实践

阐述了非物质文化遗产保护的意义和高校图书馆对参与非物质文化遗产抢救保护的优势,论述了高校图书馆在非物质文化遗产保护中的角色定位.参与非物质文化遗产保护,高校图书馆的功能可以拓展、延伸.结合实践探讨了高校图书馆参与非物质文化遗产收集、整理、传递的内容与方式.     

Protective role of phospholipid oxidation products in endotoxin-induced tissue damage

Lipopolysaccharide (LPS), an outer-membrane component of Gram-negative bacteria, interacts with LPS-binding protein and CD14, which present LPS to toll-like receptor 4 (refs 1, 2), which activates inflammatory gene expression through nuclear factor kappa B (NF kappa B) and mitogen-activated protein-kinase signalling. Antibacterial defence involves activation of neutrophils that generate reactive oxygen species capable of killing bacteria; therefore host lipid peroxidation occurs, initiated by enzymes such as NADPH oxidase and myeloperoxidase. Oxidized phospholipids are pro-inflammatory agonists promoting chronic inflammation in atherosclerosis; however, recent data suggest that they can inhibit expression of inflammatory adhesion molecules. Here we show that oxidized phospholipids inhibit LPS-induced but not tumour-necrosis factor-alpha-induced or interleukin-1 beta-induced NF kappa B-mediated upregulation of inflammatory genes, by blocking the interaction of LPS with LPS-binding protein and CD14. Moreover, in LPS-injected mice, oxidized phospholipids inhibited inflammation and protected mice from lethal endotoxin shock. Thus, in severe Gram-negative bacterial infection, endogenously formed oxidized phospholipids may function as a negative feedback to blunt innate immune responses. Furthermore, identified chemical structures capable of inhibiting the effects of endotoxins such as LPS could be used for the development of new drugs for treatment of sepsis.     

Role of toll-like receptors in regulatory functions of T and B cells

Pathogens can find their ways to most sites in the host. Pathogen sensors, such as Toll-like receptors （TLRs）, must be equally and broadly distributed on immune cells to combat them through innate and adaptive immunity. Most classes of TLRs are found in innate immune cells to obtain an immediate response against pathogens, but recent studies indicate that a number of TLRs are wildly expressed in T and B cells, suggesting TLRs also directly regulate adaptive immune responses. Due to the rapid increase of new information on the multiple roles of TLRs, in this paper we aim to review several main properties of TLRs and their direct role in T and B cells. This review consists of 6 parts： （i） Characteristics of Toll-like receptors （TLRs） and signaling; （ii） signalling pathways of TLRs; （iii） TLR expressions on human leukocytes; （iv） TLR expressions and functions in the Thl, CD4^＋CD45RO^＋ memory T cells and regulatory/suppressor T as well as B cell populations; （v） therapeutic potential of TLR agonists; （Vi） discussion and perspective. The latest findings and potential therapeutic applications are discussed. There is growing evidence supporting the concept that TLR activation contributes not only to innate immunity but also to adaptive immunity, including direct regulation of both T and B lymphocytes by TLRs.     

体外培养人角膜内皮细胞的UVB损伤及抗坏血酸的抗氧化保护作用研究

以非转染人角膜内皮(HCE)细胞系为体外实验模型系统研究了UVB氧化损伤、Asc抗氧化保护及其分子机理。体外培养的HCE细胞经UVB和/或Asc处理后,利用MTT和光镜对细胞的活力和形态进行了检测,利用8-羟基脱氧鸟苷免疫荧光染色对DNA的氧化损伤进行了检测,并利用二氢乙啶染色对胞内活性氧(ROS)的水平进行了检测。结果显示,100~800 mj/cm²的UVB辐射能剂量和时间依赖性地损伤HCE细胞的活力;200 mj/cm² UVB(自然太阳光中的平均辐射剂量)能引起HCE细胞发生皱缩,并显著增加细胞的DNA氧化损伤程度及胞内ROS水平;而1 mmol/L Asc不仅能显著增强HCE细胞的活力、促进细胞分裂,而且还能显著降低200 mj/cm² UVB所引起的DNA氧化损伤及胞内ROS水平。综上所述,UVB通过诱导ROS的产生进而引起DNA氧化损伤,对HCE细胞具有显著的氧化损伤作用;而Asc能够通过降低UVB诱导的ROS水平进而保护DNA免受氧化损伤,对HCE细胞的UVB损伤具有一定的抗氧化保护作用。本文研究结果对于利用Asc等抗氧化保护剂保护HCE细胞免受UVB氧化损伤具有一定的理论指导价值。     

Role of corticosteroid-binding globulin in interaction of corticosterone with uterine and brain progesterone receptors

The central actions of the steroid hormone progesterone remain an enigma. However, there is no doubt that this hormone has a vital role in the control of sexual function and behaviour in many species, including man. Furthermore, progesterone may be involved in the premenstrual and postpartum syndromes. It would therefore be very useful to know the role and mechanism of action of progesterone in the brain. We now show that there are differences between progesterone receptors in brain and uterus, and possibly in the distribution of the serum progesterone-binding protein, corticosteroid-binding globulin (CBG), which may enter uterine but not brain cells.