硒与甲状腺

硒是生命必需的一种微量元素.硒在体内最主要的生物活性形式是硒代半胱氨酸,以硒代半胱氨酸为活性中心的蛋白质,称为含硒蛋白.硒主要的生物学作用是抗氧化和抗炎症反应.甲状腺内含有多种含硒蛋白,其中最重要的2种为谷胱甘肽过氧化物酶和脱碘酶,前者是甲状腺组织中重要的抗氧化剂,保护甲状腺细胞免受氧化应激损伤;后者是一组与甲状腺激素代谢相关的酶.硒缺乏与多种甲状腺疾病的发生发展有关.研究表明,低硒可加重自身免疫性甲状腺疾病、增加甲状腺癌发病风险以及促进甲状腺肿的发生发展等.补硒可能具有一定治疗作用,但补硒治疗目前尚不成熟,其有效性、安全性等尚需更多的临床药物研究提供理论依据.     

硒预防心血管病的研究进展

<正>硒是人体必需的微量元素之一,是人体重要的含硒蛋白质的必要组成部分,硒具有抗炎、抗氧化应激、促进免疫调节等作用〔1〕,硒缺乏与癌症、病毒感染及多种心血管疾病等〔2〕相关。饮食补充硒等营养物质常用于保持健康和疾病预防,特别是各种慢性疾病患者。硒发挥心血管疾病保护作用的实验证据充分。本文就硒对心血管疾病的预防及作用机制作一综述。1硒的生物学特征与功能目前,人蛋白质组中已发现25种硒蛋白,常见的如谷胱甘     

血硒与慢性血管性疾病关系的研究进展

自1957年Schwarz和Flotz证实硒能够预防生物体的特异性营养缺乏状态,是生物体内的一种必需微量元素之后,硒的营养价值与机体缺硒性疾病的研究广泛受到人们重视.研究证明许多疾病的发生与发展和机体血硒含量相对缺乏有关,1973年,世界卫生组织将硒确定为人和动物生命活动的必需微量元素,1988年我国营养协会将硒列为每日膳食营养素之一,目前认为硒在体内具有抗氧化、促进免疫、清除自由基、调控基因表达、促进基础代谢等对维持机体正常的生理机能有重要的调节或保护作用[1].     

硒在动脉粥样硬化中的研究进展

动脉粥样硬化是心血管疾病最常见的病理生理机制,其病变程度决定了心血管疾病的发生发展及预后.硒是人体必需的微量元素,主要以硒蛋白的形式发挥作用,在体内参与抗氧化、抗炎、抗癌等过程.现有研究表明,硒与动脉粥样硬化的发生发展密切相关,补硒可减轻动脉粥样硬化.本文从血管内皮功能障碍,血管平滑肌异常增殖,血管钙化等促动脉粥样硬化...     

肠道微生物代谢产物氧化三甲胺与心血管疾病研究进展

近期研究发现,依赖肠道微生物的胆碱代谢产物氧化三甲胺(Trimethylamine-N-oxide,TMAO)在心血管疾病发生、发展中起着重要作用,其中患者血浆TMAO水平升高与心血管疾病呈明显正相关,经研究表明高水平的血浆TMAO导致主要不良心血管事件发生率增加。同时,TMAO与心血管疾病动脉粥样硬化、高血压病、心功能不全的研究也备受关注。本文就TMAO与心血管疾病关系的研究进展进行综述。     

氧化三甲胺与心血管疾病的研究进展

近期研究表明,肠道菌群结构紊乱不仅与消化系统疾病、内分泌系统疾病、肿瘤等相关,而且与心血管疾病的发生密切相关。肠道微生物利用富含胆碱或三甲胺结构的物质代谢生成的氧化三甲胺(trimethylamine-N-oxide,TMAO),在心血管疾病的发生和发展中起着重要作用。同时,TMAO与心血管疾病如动脉粥样硬化、心力衰竭、高血压病的研究也备受关注。最新研究证实血浆TMAO水平与不良心血管事件的发生率呈显著正相关。现就TMAO与心血管疾病关系的研究进展进行综述。     

硒对砷毒性的拮抗作用

硒(Se)是人体必需的微量元素,在生物体内具有广泛的生物学作用.硒不仅有抗氧化、增强免疫、调节代谢、降低心血管疾病发生等作用,还具有解毒功能,能拮抗砷(As)、镉(Cd)、汞(Hg)、镍(Ni)、铅(Pb)等有毒化合物对机体的损伤.有研究表明高砷地区伴有低硒,砷中毒病人血清硒含量降低.因此,深入研究硒对砷的拮抗作用,对探索砷中毒的治疗方法具有重要意义.     

CD147糖基化与心血管疾病

流行病学资料表明心血管疾病作为一种慢性疾病严重威胁大众的健康。随着我国逐渐进入人口老龄化阶段，这一问题将会更加严峻。“细胞?细胞外基质”的相互作用影响心血管疾病的发生发展，越来越多的研究结果证实，细胞外基质微环境的变化在心血管疾病的发生中扮演着重要的角色。在体内多种组织中表达的跨膜糖基化蛋白CD147，其糖基化在其功能的发挥中具有重要作用。CD147在心血管系统中可促进肺动脉高压、动脉粥样硬化和血小板活化的发生。此外，CD147还会扰乱NO代谢并导致有害的内皮活化，包括RhoA蛋白激酶活化。更重要的是，CD147在扩张型心肌病、心肌梗死和炎症性心肌病患者左心室中出现高表达。因此，CD147糖基化可能作为心血管病治疗的一种手段与方法。     

全国老年人退行性心血管疾病学术研讨会征文通知

年龄因素在器质性心血管疾病的发生及发展中有重要作用,但某些心血管疾病无其他可发现的器质性病因,因而推测这些心血管疾病属于老年人退行性心血管疾病,例如老年退行性瓣膜病、高龄患者的特发性心房颤动、Lev病等。老年人的心血管解剖学、功能学(收缩功能、舒张功能、电功能等)、生理学、生物化学等多方面会有生理性退行性变,轻者属于功能性问题,严重时则能起到致病作用,表现为疾病。国外某些研究中心的资料表明,老年患者心脏瓣膜置换术的50％病因是退行性瓣膜病。     

微量元素参与主动脉疾病发病机制的研究进展

研究表明,人体必需微量元素如铁、铜、锌、硒等在主动脉疾病如主动脉瘤和主动脉夹层患者体内存在不同程度的紊乱.本文通过检索、分析相关文献,总结了微量元素参与主动脉疾病的发病机制,其中铁、铜过载能够通过芬顿/哈伯-韦斯反应而产生过氧化物,进而对主动脉壁细胞造成氧化损伤;铁缺乏能够影响肌动蛋白的合成和肌球蛋白的磷酸化,破坏细胞...     

Selenium in rheumatic diseases

Selenium is involved in several important biochemical pathways relevant to rheumatic diseases. Experimental and clinical studies suggest that selenium modulates the inflammatory and immune responses. Patients suffering from inflammatory rheumatic diseases often have low selenium levels, but this finding does not correlate with disease severity. Selenium supplementation needs stricter selection criteria and better ascertainment of dose to obtain a stimulatory or inhibitory effect relevant to the disease state. Prevention of marginal selenium deficiency by moderate supplementation might enhance host defense mechanisms.     

Selenium deficiency

Selenium is undoubtedly an essential trace element: its involvement in GPx structure, the presence of deleterious effects of selenium deficiency in animals, and the recognition of deficiency states in man attest to its importance. However, if the consequences of selenium deficiency in man are now widely recognized, the mechanisms underlying these conditions are poorly understood. The definition of the exact role of selenium in human homeostasis has been hampered by the lack of a sensitive parameter, usable in routine investigation, to assess selenium status. Measurements of plasma and urinary levels, although useful in clinical practice, are inadequate indicators. The only true evidence of selenium deficiency lies in a positive response to selenium therapy. Deficiency states have been demonstrated for inhabitants of regions where selenium supply is limited, in protein-energy malnutrition, and in patients maintained on total parenteral nutrition without selenium supplementation. The benefit of selenium supplementation, together with other antioxidant drugs, in non-deficient subjects is still a matter of debate; its protective effect in neoplastic, cardiovascular and neurological degenerative diseases is not yet proven.     

Selenium and antioxidant defenses as major mediators in the development of chronic heart failure

Increased oxidative stress is involved in the pathogenesis of chronic heart failure (CHF), the common end result of most cardiac diseases. Selenium is an “essential” trace element, which means that it must be supplied by our daily diet and that its blood and tissue concentrations are extremely low. Selenium has a variety of functions. It is a key component of several functional selenoproteins required for normal health. The best known of these are the antioxidant glutathione peroxidase (GPx) enzymes, which remove hydrogen peroxide and the harmful lipid hydroperoxides generated in vivo by oxygen-derived species. GPx deficiency exacerbates endothelial dysfunction, a major contributing factor in the severity of CHF symptoms, in various conditions such as hyperhomocysteinemia. This suggests that homocysteine may be involved in the CHF associated endothelial dysfunction through a peroxide-dependent oxidative mechanism. Selenium also plays a role in the control of thyroid hormone metabolism and in protection against organic and inorganic mercury. One possible additional mechanism by which low selenium may compromise cardiovascular condition may be through the effect of selenium on the synthesis and activity of deiodinases, enzymes converting thyroxin into the biologically active triiodothyronine. Selenium and iodine actually interact in cardiovascular physiology, and further studies are needed to examine their role, in isolation and in association, in the development of CHF. Thus, selenium (through its role in selenoenzymes, thyroid hormones, and interactions with homocysteine and endothelial function) appears to be a major mediator in several pathways potentially contributing to CHF development.     

Selenium deficiency and fatal cardiomyopathy in a patient on home parenteral nutrition

An adult patient with chronic idiopathic intestinal pseudo-obstruction maintained on home parenteral nutrition for 6 consecutive years died from cardiomyopathy and ventricular fibrillation. Postmortem examination of the heart revealed widespread myocytolysis and replacement fibrosis similar to that seen in the selenium deficient cardiomyopathy in China (Keshan disease) and animal models. Selenium deficiency in this patient was documented with extremely low concentrations of selenium and decreased activity of the selenoprotein, glutathione peroxidase, in blood, heart, liver, and skeletal muscle. Reports of selenium deficient diets causing myocardial damage in humans and animals and the findings in our patient strongly suggest that his fatal cardiomyopathy was caused by selenium deficiency.     

Disappearance of Gastritis after Eradication of Helicobacter pylori: A Morphometric Study

Background: Patients with intestinal disease are at risk of developing selenium deficiency due to impaired intestinal absorption. The aim of the present study was to evaluate selenium status and to identify predictive factors of selenium depletion in patients with gastrointestinal disease. Methods: The concentration of selenium and the activity of glutathione peroxidase in plasma and erythrocytes were measured by fluorometry and by spectrophotometry. Eighty-six patients with Crohn's disease, 40 patients with ulcerative colitis, and 39 patients with various other gastrointestinal diseases were studied. Twenty-seven patients (16%) received home parenteral nutrition. Stool mass, faecal fat, and vitamin B₁₂ absorption were analysed in 100 patients. Results: The plasma selenium concentration was decreased in 85% of the patients receiving supplementary parenteral nutrition and in 20% of the patients receiving oral nutrition, among them in 26% of the patients with Crohn's disease. Almost all patients with ulcerative colitis had normal selenium levels. A statistically significant correlation was found between plasma selenium and vitamin B₁₂ absorption, stool mass, faecal fat excretion, body mass index, P-albumin, P-zinc, and the length of the remaining small bowel. Stepwise regression analyses showed that the strongest predictors of selenium deficiency were stool mass, vitamin B₁₂ absorption, and the length of the small-bowel resection. _Conclusion: Selenium deficiency is common in patients with severe gastrointestinal disorders. The deficiency is mainly related to malabsorption, and a low selenium level was almost invariably present in patients who needed parenteral supplementation due to gut failure.     

Selenium is depleted in Crohn's disease on enteral nutrition

BACKGROUD/AIMS: Selenium is an important trace element and its deficiency has been reported to be associated with cardiomyopathy or gastrointestinal cancer. The aim of this study is to clarify the selenium status in Crohn's disease (CD) on enteral nutrition. METHODS: We measured serum selenium concentrations in 53 patients with CD and compared them with those in 21 healthy controls. Twenty-nine patients were under the treatment by enteral nutrition (EN group), and the remaining 24 patients were free from formulated enteral nutrition (non-EN group). RESULTS: While the serum selenium concentration in the non-EN group was not decreased when compared to controls, the value in the EN group was significantly lower than those in the non-EN group and in controls. Clinical manifestations of selenium deficiency were found in a patient on exclusive enteral nutrition. In the EN group, the serum selenium concentration showed an inverse correlation with the duration and the daily dose of enteral nutrition. In the non-EN group, the serum selenium concentrations were inversely correlated with the Crohn's disease activity index. CONCLUSION: These findings suggest that patients with CD on enteral nutrition are at risk for selenium deficiency and that even patients without enteral nutrition may develop selenium deficiency at the active phase of the disease.     

Decreased hepatic selenium content in alcoholic cirrhosis

Selenium deficiency has been implicated as contributing to hepatic injury in alcoholics. The mechanism by which this occurs is most likely lipoperoxidation secondary to decreased activity of the selenoenzyme glutathione peroxidase. To further assess this relationship, we measured selenium content in autopsy livers in 12 patients with alcoholic cirrhosis compared to 13 patients matched for age and sex dying from other causes, mostly with cardiopulmonary diseases. The mean (±sem) hepatic selenium content in cirrhosis was 0.731±0.077 Μg/g dry weight versus 1.309±0.166 Μg/g in controls (P< 0.005; Student's t test). Clinical and biochemical indices of significant hepatic dysfunction, including encephalopathy, ascites, and elevations of serum bilirubin or prothrombin time, were only present in the cirrhotic group. A significant inverse correlation between hepatic selenium content and the prothrombin time was noted (r=?0.50; Ps<0.02). No significant relationships between hepatic selenium and the abnormalities of bilirubin, albumin, or aspartate aminotransferase were found. We conclude that significantly decreased hepatic selenium stores are present in patients with severe alcoholic cirrhosis compared to controls. The magnitude of that selenium deficit does correlate with some indices of hepatic function, specifically the prothrombin time. These data lend further support to a true selenium deficiency state in alcoholic cirrhosis. It is highly possible that selenium deficiency represents an important link, synergistically joining the nutritional and hepatotoxic backgrounds of alcoholic liver injury and cirrhosis.     

Selenium, selenoproteins and the thyroid gland: interactions in health and disease

The trace element selenium is an essential micronutrient that is required for the biosynthesis of selenocysteine-containing selenoproteins. Most of the known selenoproteins are expressed in the thyroid gland, including some with still unknown functions. Among the well-characterized selenoproteins are the iodothyronine deiodinases, glutathione peroxidases and thioredoxin reductases, enzymes involved in thyroid hormone metabolism, regulation of redox state and protection from oxidative damage. Selenium content in selenium-sensitive tissues such as the liver, kidney or muscle and expression of nonessential selenoproteins, such as the glutathione peroxidases GPx1 and GPx3, is controlled by nutritional supply. The thyroid gland is, however, largely independent from dietary selenium intake and thyroid selenoproteins are preferentially expressed. As a consequence, no explicit effects on thyroid hormone profiles are observed in healthy individuals undergoing selenium supplementation. However, low selenium status correlates with risk of goiter and multiple nodules in European women. Some clinical studies have demonstrated that selenium-deficient patients with autoimmune thyroid disease benefit from selenium supplementation, although the data are conflicting and many parameters must still be defined. The baseline selenium status of an individual could constitute the most important parameter modifying the outcome of selenium supplementation, which might primarily disrupt self-amplifying cycles of the endocrine-immune system interface rectifying the interaction of lymphocytes with thyroid autoantigens. Selenium deficiency is likely to constitute a risk factor for a feedforward derangement of the immune system-thyroid interaction, while selenium supplementation appears to dampen the self-amplifying nature of this derailed interaction.     

Impact of intensive statin therapy on hs-CRP and sCD40L in AMI patients during perioperative period of emergency PCI

Background It's an effective treatment to achieve percutaneous coronary intervention(PCI) in acute myocardial infarction(AMI) patients for reperfusion of coronary artery.The PCI treatment can improve the blood supply of coronary artery,make some adverse effects at the same time.Studies have shown that statins have other effects in addition to lipid-lowering,such as anti-inflammatory effects.It can significantly reduce the incidence of coronary heart disease,cardiovascular disease mortality and even all-caus...     

Lipid-lowering therapy for elderly patients at risk for coronary events and stroke

Hyperlipidemia continues to be a major risk factor for cardiovascular diseases, particularly coronary heart disease, in the elderly population. Despite the fact that hyperlipidemia does not seem to be a major risk factor for stroke, therapy for hyperlipidemia, especially with statins, has clearly been demonstrated to reduce both coronary heart disease events and stroke, with the most convincing data being for the elderly population. Although we review some safety concerns with statin therapy applicable to the elderly, statins alone or with other proved therapies, including fibrates, niacin, and exercise training, have been demonstrated to reduce major cardiovascular diseases, including coronary heart disease and stroke in the elderly. In addition, this therapy can be safely administered to most elderly patients and seems to have either neutral or slightly beneficial effects on dementia. Therefore, aggressive lipid treatment, particularly with statins, is needed in the primary and secondary prevention of cardiovascular diseases in the elderly.