褪黑素对急性坏死性胰腺炎合并肾损伤的保护作用及机制研究

急性肾功能衰竭是重症急性胰腺炎(SAP)患者早期病死的主要原因之一.因此研究其发病机制并寻求有效的防治措施具有重要的临床价值.Ghrelin是生长激素促分泌物受体的内源性配体,它在急性胰腺炎(AP)发生发展中具有抑制炎症的作用.本研究应用褪黑素干预急性坏死性胰腺炎(ANP)大鼠,观察肾组织Ghrelin和NF-κB p65表达及肾组织中氧化应激相关指标的变化,探讨褪黑素对肾损伤的作用机制.     

褪黑素对胰腺炎损伤的剂量依赖性保护作用的研究进展

褪黑素是一种具有抗氧化作用和免疫调节作用的吲哚类激素,它可以下调急性炎性反应过程中多种炎性介质的表达,从而减轻各个脏器的急性炎性反应.实验研究表明,褪黑素不仅在急性胰腺炎(AP)及相关性脏器损伤中发挥着保护作用,而且这一作用具有剂量依赖性和昼夜节律性.此文对这一方面的研究进展作一综述.     

缺氧诱导因子-1与急性肺损伤

急性肺损伤发病机制复杂,目前认为肺内过度炎症反应是其发病的关键环节.缺氧诱导因子-1是一种氧依赖转录激活因子,也参与急慢性炎症反应,已证实缺氧诱导因子-1在急性肺损伤过程中起着重要作用.本文就缺氧诱导因子1在肺损伤急性炎症反应及损伤后的修复过程中所扮演的角色作一综述.     

褪黑素腹腔注射对急性脑梗死大鼠神经细胞损伤凋亡的改善作用及其机制

目的 观察褪黑素腹腔注射对急性脑梗死大鼠神经细胞损伤凋亡的改善作用,并探讨其机制.方法 60只SD大鼠随机分为假手术组、模型组、褪黑素低剂量组、褪黑素中剂量组、褪黑素高剂量组、阳性对照组,每组10只.除假手术组外,其他5组建立急性脑梗死模型.造模成功后开始给药,褪黑素低剂量组、褪黑素中剂量组、褪黑素高剂量组分别给予褪黑...     

高密度脂蛋白抗炎症到促炎症的转变

高密度脂蛋白具有抗炎症的特性.高密度脂蛋白促进胆固醇外流的功能对预防心血管疾病有重要的作用,同样,其抗炎症特性也具有非常重要的作用.高密度脂蛋白在免疫系统中发挥着重要的作用,在不发生急性相反应的条件下能发挥抗炎症作用,反之,则有促进炎症发生的作用.高密度脂蛋白的抗炎症特性主要是其内容物所决定的,在发生急性相反应时,其组成成分发生改变,从而促进了高密度脂蛋白从抗炎症到促炎症的转变.     

褪黑素与急性胃粘膜病变

褪黑素是机体正常情况下分泌的一种神经内分泌激素 ,具有广泛的生理功能 ,并且能参与机体许多疾病或损伤的保护反应。近年来 ,在胃肠道中的作用逐步受到重视 ,尤其在急性胃粘膜的损害中发挥了重要作用。     

心肌梗死早期舒降之治疗对C反应蛋白的影响

C反应蛋白(C-reactive protein,CRP)是一种急性炎症时相反应蛋白,属非特异性反应蛋白,而炎症与免疫在动脉粥样硬化的发生、发展中起重要作用.CRP与动脉粥样硬化、冠状动脉疾病的发生发展和预后有着密切的关系[1].急性心肌梗死早期大剂量辛伐他汀(舒降之-默沙东制药)治疗可降低CRP的水平,抑制炎症反应、稳定粥样硬化斑快.     

C反应蛋白与慢性阻塞性肺疾病

C反应蛋白是在机体炎症、感染或组织损伤时,由一种肝细胞合成释放的急性时相反应蛋白.在众多慢性阻塞性肺疾病患者血清中水平增加的炎症因子中,C反应蛋白是研究最多的一种.本文重点针对C反应蛋白在慢性阻塞性肺疾病中的作用方面的进展进行阐述.     

一氧化氮在急性肺损伤炎症反应中的双向调节作用

炎症反应在急性肺损伤中发挥了重要作用,一氧化氮通过核因子途径以及一氧化氮合酶途径参与炎症反应的调节,但不同剂量的一氧化氮对炎症反应产生不同的作用。高浓度的一氧化氮可以抑制急性肺损伤时的炎症反应,减轻组织的损伤。而低浓度的一氧化氮则促进炎症反应的发展,加重组织的损伤。     

褪黑素与急性胃粘膜病变

褪黑素是机体正常情况下分泌的一种神经内分泌激素，具有广泛的生理功能，并且能参与机体许多疾病或损伤的保护反应。近年来，在胃肠道中的作用逐步受到重视，尤其在急性胃粘膜的损害中发挥了重要作用。     

The effects of physical activity on serum C-reactive protein and inflammatory markers: a systematic review

Physical activity is associated with a reduced incidence of coronary disease, but the mechanisms mediating this effect are not defined. There has been considerable recent interest in inflammation in the pathogenesis of cardiovascular disease. Some of the beneficial role of physical activity may result from its effects on the inflammatory process. We searched PubMed for articles published between 1975 through May 2004 using the terms exercise, physical activity, or physical fitness combined with C-reactive protein, inflammation, inflammatory markers, or cytokines. The review revealed 19 articles on the acute inflammatory response to exercise, 18 on cross-sectional comparisons of subjects by activity levels, and 5 examining prospectively the effects of exercise training on the inflammatory process. Exercise produces a short-term, inflammatory response, whereas both cross-sectional comparisons and longitudinal exercise training studies demonstrate a long-term "anti-inflammatory" effect. This anti-inflammatory response may contribute to the beneficial effects of habitual physical activity.     

抗细胞因子治疗心力衰竭的研究进展

近年来 ,炎性细胞因子在心力衰竭发展中的作用已成为研究热点。有研究证实 ,抗细胞因子治疗可以减缓心力衰竭进程。因此 ,为了明确炎性细胞因子在心力衰竭病理生理发生机制中的作用 ,就以下几个方面作简要介绍 :炎性细胞因子的生物学特性及其对心脏重塑及心力衰竭发生发展的影响 ,目前抗细胞因子治疗心力衰竭策略的现状。     

Effect of a specific iron chelating agent on animal models of inflammation.

Iron is an important catalyst of oxidative radical reactions and promotes the formation of the hydroxyl radical from the superoxide anion radical and hydrogen peroxide. The stimulatory effect of the hydroxyl radical on lipid peroxidation prompted the speculation that free iron may directly promote inflammation and that iron chelating agents may have useful anti-inflammatory properties. This hypothesis is tested in animal models of inflammation with a specific iron chelating agent, desferrioxamine. At low doses (6 . 6 mg/kg) intraperitoneal desferrioxamine stimulated the induction of acute foot pad swelling in rats by monosodium urate but at higher doses (above 200 mg/kg) it suppressed this inflammatory reaction. A similar anti-inflammatory effect was observed in carrageenan-induced foot pad swelling. In guinea-pigs in which a Glynn-Dumonde synovitis was induced with bovine gammaglobulin, desferrioxamine (100 mg/kg) stimulated the acute inflammatory induction phase of this chronic allergic monoarthritis model. Repeated administration of desferrioxamine (100 mg/kg) from the seventh to the twelfth day after intra-articular challenge with bovine gammaglobulin markedly depressed the chronic inflammatory phase. In-vitro experiments suggest that desferrioxamine inhibits iron-catalysed lipid peroxidation when it is poorly saturated with iron, but loses this effect when it is iron saturated. Such an effect may explain our results with desferrioxamine in the animal studies and suggests that effective iron chelation and its removal may modify the inflammatory process in man.     

丁酸钠对TNBS结肠炎模型大鼠肠黏膜修复的影响

背景：肠道黏膜的炎症损伤和修复是炎症性肠病（IBD）的重要特征之-。丁酸盐为肠上皮细胞的主要能量来源,参与了肠道黏膜内稳态的维持并具有抗炎效应。目的：观察丁酸钠对结肠炎模型大鼠肠黏膜炎症损伤和修复的影响．探讨其治疗IBD的可能机制。方法：以三硝基苯磺酸（TNBS）诱导大鼠结肠炎模型并予丁酸钠或美沙拉嗪治疗,同时设置正常对照组和结肠炎模型组。于急、慢性炎症期分批处死大鼠,行结肠组织学检查和评分,免疫组化方法检测结肠组织中与黏膜修复相关的转化生长因子-β1（TGF-β1）、血管内皮生长因子（VEGF）表达,ELISA方法检测血浆促炎细胞因子白细胞介素．8（IL-8）、抗炎细胞因子IL-10水平。结果：与结肠炎模型组相比,丁酸钠治疗组一般情况和结肠组织学表现有所改善．美沙拉嗪治疗组则有明显改善。丁酸钠治疗组和美沙拉嗪治疗组结肠组织TGF—β1阳性表达率显著高于结肠炎模型组（P〈0．05）,VEGF阳性表达率无明显变化．慢性炎症期血浆IL_8水平显著降低（P〈0．05）．IL-10水平显著增高（P〈0．05）。结论：丁酸钠对TNBS结肠炎模型大鼠的肠黏膜修复有-定促进作用,该作用可能与其增加TGF-β1表达和调节促炎细胞因子与抗炎细胞因子平衡有关。     

Inflammatory markers and stroke

Basic and animal research implicate inflammatory mechanisms in the pathogenesis and progression of atherosclerosis, plaque rupture, thrombosis, and stroke. Inflammatory biomarkers, particularly high-sensitivity C-reactive protein and lipoproteinassociated phospholipase A2, have been identified as potential predictors of stroke risk and prognosis. Infections may also precipitate stroke. Medications, especially hydroxymethylglutaryl coenzyme A reductase inhibitors (statins), reduce inflammatory marker levels independently of lipid effects, and the ability of statins to reduce coronary events and stroke correlates with their effect on inflammatory biomarkers. Vaccination against influenza may also reduce stroke risk. Determining whether reduction of biomarkers reduces risk of recurrent stroke, however, requires further study before inflammatory markers become a routine part of the evaluation of stroke patients.     

人血清胎球蛋白A在COPD中的作用

COPD是一种慢性炎症性疾病,这种持续低水平的系统性炎症可能与其并发症,如心血管疾病、代谢综合征、骨质疏松等有密切关系.人血清胎球蛋白A具有抗炎及抑制血管钙化的生物学作用,可能与COPD的炎症反应及其合并症有关,认识人血清胎球蛋白A在COPD中的作用,可能为COPD患者的诊断和治疗提供新的思路.     

Pharmacogenetics and anti-inflammatory effect of HMG-CoA reductase inhibitors

Atherosclerosis is a result from the association of lipid deposition in the arterial wall and inflammatory process. This inflammatory process may be detected by clinical markers of systemic inflammation, such as ultrasensible C-reactive protein, which is associated with cardiovascular risk, independently of lipid levels. Statins reduce the inflammation associated to atherosclerosis, which may be verified by a reduction of the C-reactive protein levels. It seems that statins alter immune function by modulating post-translational protein prenylation. Individual genetic variations are associated with modulation of statins lipid-lowering effect; however, few studies have related the effect of the genetic variants with anti-inflammatory effect of statins. In addition to the genes involved in the cholesterol metabolism, genetic factors affecting statins pharmacodynamics and/or pharmacokinetics are potentially responsible for lipid and anti-inflammatory effects.     

Nutrition in inflammatory bowel disease

Nutrition is clearly disturbed by active intestinal inflammation. Appetite is reduced, yet energy substrates are diverted into the inflammatory process, and thus weight loss is characteristic. The nutritional disturbance represents part of a profound defect of somatic function. Linear growth and pubertal development in children are notably retarded, body composition is altered, and there may be significant psychosocial disturbance. Macrophage products such as tumour necrosis factor-alpha and interleukins-1 and 6 may be the central molecules that link the inflammatory process to this derangement of homeostasis. Intriguingly, there is also increasing evidence that an aggressive nutritional programme may in itself be sufficient to reduce the mucosal inflammatory response. Recent evidence suggests that enteral nutrition alone may reduce many pro-inflammatory cytokines to normal and allow mucosal healing. In addition, specific nutritional components, such as n-3 polyunsaturated fatty acids, may have an anti-inflammatory effect as they may alter the pattern of leukotrienes generated during the immune response. The recent discovery of the specific molecular mediators of appetite and body composition, such as leptin and myostatin, may allow increased therapeutic specificity and further improvement in the nutritional treatment of the inflammatory bowel diseases.     

Pregnancy and inflammatory bowel disease

Overall, around 25% of women with inflammatory bowel disease will conceive during their disease. Most of the women with inflammatory bowel disease will have a normal pregnancy and healthy children. However, specific problems may arise related to these pregnancies. This paper reviews what is known on fertility, risk of disease transmission, effect of the disease on the pregnancy and the reverse, delivery, medical follow up and treatment as well as breastfeeding in the setting of inflammatory bowel disease.     

Partial chondroprotective effect of zoledronate in a rabbit model of inflammatory arthritis.

OBJECTIVE: To test the hypothesis that bisphosphonate treatment has a chondroprotective effect in the carrageenan model of inflammatory arthritis (IA). METHODS: Experimental IA was induced in rabbits by intraarticular injections of carrageenan. One group also received subcutaneous injections of zoledronate, a new bisphosphonate. After 4 weeks, the joints were harvested. Articular cartilage degradation and the degree of synovitis were assessed by light microscope using qualitative grading scores. Articular cartilage and subchondral and cancellous bone were evaluated histomorphometrically. Bone microhardness was measured. RESULTS: Carrageenan injected knees showed changes of inflammatory arthritis with cartilage erosion. Zoledronate treatment partially protected the articular cartilage from degradation. This effect was unlikely due to an antiinflammatory effect of the drug as the carrageenan induced synovitis was unaffected by zoledronate treatment. The treatment preserved subchondral bone thickness and cancellous bone volume and prevented focal breaks in the osteochondral barrier. The subchondral bone hardness was also maintained. CONCLUSION: Zoledronate had a partial effect in a rabbit model of inflammatory arthritis. The chondroprotection may be due to the prevention of bone resorption. By maintaining an intact subchondral bone, normal joint loading may have been maintained and contact between the bone marrow and the articular cartilage averted.