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1.
The concept that atherosclerosis is an inflammation has been increasingly recognized, and subsequently resulted in great interest in revealing the inflammatory nature of the atherosclerotic process. More recently, a large body of evidence has supported the idea that inflammatory mechanisms play a pivotal role throughout all phases of atherogenesis, from endothelial dysfunction and the formation of fatty streaks to plaque destabilization and the acute coronary events due to vulnerable plaque rupture. Indeed, although triggers and pathways of inflammation are probably multiple and vary in different clinical entities of atherosclerotic disorders, an imbalance between anti-inflammatory mechanisms and pro-inflammatory factors will result in an atherosclerotic progression. Vascular endothelial dysfunction and lipoprotein retention into the arterial intima have been reported as the earliest events in atherogenesis with which inflammation is linked. Inflammatory has also been extended to the disorders of coronary microvasculature, and associated with special subsets of coronary artery disease such as silent myocardial ischemia, myocardial ischemia-reperfusion, cardiac syndrome X, variant angina, coronary artery ectasia, coronary calcification and in-stent restenosis. Inflammatory biomarkers, originally studied to better understand the pathophysiology of atherosclerosis, have generated increasing interest among researches and clinicians. The identification of inflammatory biomarkers and cellular/molecular pathways in atherosclerotic disease represent important goals in cardiovascular disease research, in particular with respect of the development of therapeutic strategies to prevent or reverse atherosclerotic diseases.
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2.
Background Glucocorticoid signaling exerts major roles in inflammation, metabolism and depression, which are three crucial factors accompanying or underlying coronary heart disease. Although accumulating evidence indicates the influence of glucocorticoids on the pathology and treatment of coronary heart disease, there is still a dearth of pharmaceutical mechanisms for this relationship. This study aimed to investigate the influence of drug treatment on glucocorticoid receptor levels in coronary heart disease. Methods Eighty hospitalized patients (average age (59.0+7.5) years, 46 male and 34 female) with coronary heart disease were categorized into four groups with 20 members in each according to one of the four drugs they were treated with. The four drugs were: nitrated derivative isosorbide dinitrate, the beta-adrenergic receptor blocker metoprolol, the calcium antagonist nifedipine, and the HMG-CoA reductase inhibitor Iovastatin. Glucocorticoid receptor protein levels of peripheral blood lymphocytes were tested using immunoblotting analysis before and after one month of treatment. Results Immunoblotting analysis showed increased glucocorticoid receptor levels after treatment with metoprolol and nifedipine. There were no statistically significant changes of glucocorticoid receptor levels after treatment with isosorbide dinitrate or Iovastatin, although there were trends of up-regulation of glucocorticoid receptor expression after both treatments. Conclusions Both the beta-blocker and the calcium blocker can increase glucocorticoid receptor levels after chronic administration. This effect suggests a mechanism for their anti-inflammatory and other therapeutic roles for coronary heart disease and comorbid disorders.  相似文献   

3.
Objective This review focuses on the role of the large conductance calcium-activated potassium (BKCa) channels in diabetic vascular complications.Data sources Relevant articles published in English or Chinese from 1981 to present were selected from PubMed.The search terms were "BKCa channels" and "diabetes".Important references from selected articles were also retrieved.Study selection Articles regarding the role of BKCa channels in diabetic vascular complications and relevant mechanisms were selected.Results The BKCa channels are abundantly expressed in vascular smooth cells and play an important role in regulation of vascular tone.Multiple studies indicated that the expression and function of BKCa channels are altered by different mechanisms in diabetic vascular diseases such as coronary arterial disease,cerebral arterial disease,and diabetic retinopathy.Conclusion BKCa channels may play an important role in diabetic vascular complications and may be an effective therapeutic target for relieving and reducing the burden of diabetic vascular complications.  相似文献   

4.
Objective To reveal the roles of Rho kinase (ROCK) in the mechanisms of complications in diabetes by reviewing the correlations between ROCK and related complications in diabetes.Data sources The data used in the present article were mainly from PubMed with relevant English articles published from 1998 to 2010. The search terms were "ROCK" and "diabetes".Study selection Original articles including the roles of ROCK or its inhibitors in diabetic complications and review articles about the biological character of ROCK were selected.Results The activity and expression of ROCK were up-regulated in the models of type 1 or type 2 diabetes animals and the cultured cells with concentrations of high glucose, ROCK activation was associated with the development or progression of complications in diabetes. Inhibition of RhoA/ROCK pathway prevented or ameliorated the pathologic changes of diabetic complications, and ROCK has been regarded as a key target for treatment of these complications.Conclusion RhoA/ROCK signaling plays important roles in the pathogenesis of long-term complications in diabetes and ROCK inhibitors are becoming a promising solution to treatments of complications in diabetes.  相似文献   

5.
The inflammation factors and roles of them in acute coronary syndrome(ACS)were explored. The similarity between the theory of pathogenic toxin in Chinese Medicine and the inflammation response theory in ACS was discussed.The exploration of new inflammatory factors may be helpful for Chinese Medicine in the research of ACS.  相似文献   

6.
Objective To review the experimental drugs for the treatment of autoimmune myocarditis.Data sources The literatures published in English about different kinds of experimental drugs based on different therapeutic mechanisms for the treatment of autoimmune myocarditis were obtained from PubMed from 2002 to 2013.Study selection Original articles regarding the experimental drugs for treatment of autoimmune myocarditis were selected.Results This study summarized the effects of the experimental drugs for the treatment of autoimmune myocarditis,such as immunomodulators and immunosuppressants,antibiotics,Chinese medicinal herbs,cardiovascular diseases treatment drugs,etc.These drugs can significantly attenuate autoimmune myocarditis-induced inflammation and fibrosis,alleviate autoimmune myocarditis-triggered overt lymphocyte proliferation,and meanwhile reduce Th1 cytokines (IFN-γ and IL-2) and increase Th2 cytokines (IL-4 and IL-10).Conclusion This study summarized recent advances in autoimmune myocarditis treatment and further proposes that traditional Chinese medicine and immune regulators will play important roles in the future.  相似文献   

7.
Pharmacological action and mechanisms of ginkgolide B   总被引:7,自引:1,他引:6  
Objective To review the recent research progress in pharmacological actions and mechanisms of ginkgolide B. Data sources Information included in this article was identified by searching of PUBMED (1987-2006) online resources using the key terms "ginkgolide B", "platelet activating factor", and "pharmacological". Study selection Mainly original milestone articles and critical reviews written by major pioneer investigators of the field were selected. Results The key issues related to the pharmacological actions and mechanisms of ginkgolide B were summarized. The ginkgolide B possesses a number of beneficial effects such as anti-inflammatory, anti-allergic, antioxidant, and neuroprotective effects. Meantime, their mechaniams were discussed. Conclusions The Ginkgolide B is the most potent antagonist of platelet activating factor (PAF) and exhibits therapeutic action in a variety of diseases mainly by the PAF receptor.  相似文献   

8.
Objective To summarize limitations involved in arsenic trioxide therapeutic effects in acute promyelocytic leukemia, because current studies show that some individuals of acute promyelocytic leukemia have relatively poor outcomes during treatment with arsenic trioxide. Data sources Most relevant articles were included in the PubMed database between 2000 and 2013 with the keywords "acute promyelocytic leukemia", "arsenic trioxide", "thiol" or "methylation". In addition, a few older articles were also reviewed. Study selection Data and articles related to arsenic trioxide effect in acute promyelocytic leukemia treatment were selected and reviewed. We developed an overview of limitations associated with arsenic trioxide therapeutic effect. Results This review focuses on the researches about the arsenic trioxide therapeutic effect in acute promyelocytic leukemia and summarizes three mainly limitations which can influence the arsenic trioxide therapeutic effect to different degrees. First, with the combination of arsenic and glutathione the therapeutic effect and cytotoxicity decrease when glutathione concentration increases; second, arsenic methylation, stable arsenic methylation products weaken the apoptosis effect of arsenic trioxide in leukemia cells; third, gene mutations affect the sensitivity of tumor cells to arsenic trioxide and increase the resistance of leukemia cells to arsenic trioxide. Conclusions The chief limitations are listed in the review. If we can exclude all of them, we can obtain a better therapeutic effect of arsenic trioxide in patients with acute promyelocytic leukemia.  相似文献   

9.
Background A variety of inflammatory mediators and effector cells participate together in acute lung injury,and lead to secondary injury that is due to an inflammatory cascade and secondary diffuse lung parenchyma injury.Inflammation is associated with an oxidative stress reaction,which is produced in the development of airway inflammation,and which has positive feedback on inflammation itself.Resolvin D1 can reduce the infiltration of neutrophils,regulate cytokine levels and reduce the inflammation reaction,and thereby promote the resolution of inflammation.The purpose of this study is to investigate the effects of resolvin D1 on an inflammatory response and oxidative stress during lipopolysaccharide (LPS)-induced acute lung injury.Methods LPS (3 mg/kg) was used to induce the acute lung injury model.Pretreatment resolvin D1 (100 ng/mouse) was given to mice 30 minutes before inducing acute lung injury.Mice were observed at 6 hours,12 hours,1 day,2 days,3 days,4 days and 7 days after LPS was administrated,then they were humanely sacrificed.We collected bronchoalveolar lavage fluid (BALF) and the lung tissues for further analysis.Paraffin section and HE staining of the lung tissues were made for histopathology observations.Parts of the lung tissues were evaluated for wet-to-dry (W/D) weight ratio.tumor necrosis factor (TNF)-α,inter leukin (IL)-1β,IL-10 and myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA).A lipid peroxidation malondialdehyde (MDA) assay kit was used to detect MDA.A total superoxide dismutase assay kit with WST-1 was used to analyze superoxide dismutase (SOD).We determined the apoptosis of neutrophils by Flow Cytometry.A real-time quantitative PCR Detecting System detected the expression of mRNA for heme oxygenase (HO)-1.Results Pretreatment with resolvin D1 reduced the pathological damage in the lung,decreased the recruitment of neutrophils and stimulated their apoptosis.It markedly decreased the expressions of TNF-α,IL-1β and increased the expressions of IL-10,and decreased the production of MDA and increased the expressions of SOD.The mRNA expression of HO-1 was also significantly increased.Conclusions Resolvin D1 displays potent anti-inflammatory actions by regulating cytokines,inhibiting aberrant neutrophil recruitment and stimulating apoptosis of neutrophils.Resolvin D1 can also relieve the injury due to oxidative stress.The mechanisms might be related to increase HO-1 expression.  相似文献   

10.
Most cases of acute coronary syndrome (ACS) involve coronary atherosclerosis and plaque rupture, as well as subsequent thrombosis. The initial thrombotic events leading to red thrombus formation are platelet adherence and aggregation. Platelets play a very important role during the establishment and progression of a thrombosis in a coronary artery. Therefore, in recent years guidelines have been developed in an effort to strengthen antiplatelet therapy in ACS, but unfortunately the methods to evaluate platelet activity and the strength of platelet inhibition are lacking.  相似文献   

11.
Vorchheimer DA  Badimon JJ  Fuster V 《JAMA》1999,281(15):1407-1414
CONTEXT: Thrombus formation on disrupted atherosclerotic plaque is the major cause of acute coronary events. Platelet inhibitors are the mainstay of drug therapy to reduce cardiac events in patients with acute coronary syndromes. The platelet glycoprotein (GP) IIb/IIIa receptor is the final common pathway of platelet aggregation. OBJECTIVES: To review mechanisms of platelet activation and aggregation and the role of the GP IIb/IIIa receptor in the acute coronary syndromes and to summarize completed clinical trials of GP IIb/IIIa receptor antagonists. DATA SOURCES: English-language journal articles, reviews from a MEDLINE search from 1993 through 1998, as well as abstracts and presentations from major national or international cardiology meetings through November 1998. STUDY SELECTION/DATA EXTRACTION: Randomized, placebo-controlled clinical trials testing intravenous GP IIb/IIIa receptor antagonists and having more than 500 subjects were included. Data quality and validity included publication or presentation venue. DATA SYNTHESIS/CONCLUSIONS: The GP IIb/IIIa receptor is the final common pathway of platelet aggregation. Intravenous monoclonal antibody and peptide and nonpeptide antagonists of the GP IIb/IIIa receptor have been tested in randomized, placebo-controlled trials of the acute coronary syndromes and percutaneous coronary interventions. For patients undergoing percutaneous revascularization, these agents have demonstrated efficacy in reducing death, myocardial infarction, or urgent reintervention. Odds ratios of death or myocardial infarction at 30 days range from 0.42 to 0.84 for the drugs in these studies. More modest benefits have been seen in trials of IIb/IIIa receptor antagonists for patients with the acute coronary syndromes, with odds ratios for death or myocardial infarction at 30 days ranging from 0.70 to 0.89. The efficacy of oral agents for chronic GP IIb/IIIa receptor antagonism has not been sufficiently studied.  相似文献   

12.

Objective:

To review the functional mechanism of apolipoprotein J (apoJ) in the process of atherosclerosis and the feasibility of apoJ as a therapeutic endpoint.

Data Sources:

Relevant articles published in English from 1983 to present were selected from PubMed. The terms of “atherosclerosis, apolipoprotein J, clusterin (CLU), oxidative stress, and inflammation” were used for searching.

Study Selection:

Articles studying the role of apoJ with atherosclerosis and restenosis after injury were reviewed. Articles focusing on the intrinsic determinants of atherosclerosis were selected. The exclusion criteria of articles were that the studies on immunologic vasculitis.

Results:

ApoJ, involved in numerous physiological process important for lipid transportation and vascular smooth muscle cell differentiation, including apoptotic cell death, cell-cycle regulation, cell adhesion, tissue remodeling, immune system regulation, and oxidative stress, plays a role in the development of clinical atherosclerosis. In the process of relieving atherosclerosis, apoJ can promote cholesterol and phospholipid export from macrophage-foam cells, and exhibit cytoprotective and anti-inflammatory actions by interacting with lots of known inflammatory proteins which may predict the onset of clinical cardiovascular events and may actually play a causal role in mediating atherosclerotic disease such as C-reactive protein, paraoxonase, and leptin. As known as CLU, apoJ has been identified to play central roles in the process of vascular smooth cells migration, adhesion, and proliferation, which can contribute significantly to restenosis after vascular injury.

Conclusions:

Intense effort and substantial progress have been made to identify the apoJ that relieves atherosclerosis and vascular restenosis after percutaneous coronary intervention. More work is needed to elucidate the exact mechanisms of and the interrelationship between the actions of apoJ and to successfully achieve regression of atherosclerosis by regarding it as a therapeutic endpoint.  相似文献   

13.
石先辉  贾如意 《医学综述》2008,14(12):1888-1890
近年来研究发现,他汀类药物不仅具有降脂作用,而且在急性冠状动脉综合征中还具有抗炎作用。阿托伐他汀作为新一代他汀类新药在调节免疫抑制炎症方面具有更好的疗效,在阻止动脉硬化的发生、发展过程中,以及在急性冠状动脉综合征预防、早期治疗、后期延缓终末事件的发生中有明显的治疗效果,这种抗炎作用是独立于降脂作用之外的,其临床应用剂量国内外差异较大,应注意合理应用。  相似文献   

14.
 氧化应激和炎症参与多种疾病的病理过程,包括代谢性疾病,如糖尿病、脂代谢紊乱、代谢综合征、肥胖和动脉粥样硬化等。目前多数抗氧化及抗炎药物剂量窗较窄、毒性较大,因此临床需要一种更加有效、安全的抗氧化应激及抗炎药物。近期大量研究提示氢分子具有选择性抗氧化及抗炎作用,对多种缺血再灌注损伤、炎症、神经疾病、消化疾病及代谢性疾病的动物模型均有很好的效果,提示氢分子有作为临床治疗代谢性疾病药物的潜能。本文综述了最新的相关研究并对未来研究方向作了展望。  相似文献   

15.
Diabetes and atherosclerosis: epidemiology,pathophysiology, and management   总被引:56,自引:1,他引:55  
Beckman JA  Creager MA  Libby P 《JAMA》2002,287(19):2570-2581
CONTEXT: Complications of atherosclerosis cause most morbidity and mortality in patients with diabetes mellitus. Despite the frequency and severity of disease, proven medical therapy remains incompletely understood and underused. OBJECTIVE: To review the epidemiology, pathophysiology, and medical and invasive treatment of atherosclerosis in patients with diabetes mellitus. DATA SOURCES: Using the index terms diabetes mellitus, myocardial infarction, peripheral vascular diseases, cerebrovascular accident, endothelium, vascular smooth muscle, platelets, thrombosis, cholesterol, hypertension, hyperglycemia, insulin, angioplasty, and coronary artery bypass, we searched the MEDLINE and EMBASE databases from 1976 to 2001. Additional data sources included bibliographies of identified articles and preliminary data presented at recent cardiology conferences. STUDY SELECTION: We selected original investigations and reviews of the epidemiology, pathophysiology, and therapy of atherosclerosis in diabetes. We selected randomized, double-blind, controlled studies, when available, to support therapeutic recommendations. Criteria for data inclusion (168 of 396) included publication in a peer-reviewed journal or presentation at a national cardiovascular society-sponsored meeting. DATA EXTRACTION: Data quality was determined by publication in peer-reviewed literature. Data extraction was performed by one of the authors. DATA SYNTHESIS: Diabetes mellitus markedly increases the risk of myocardial infarction, stroke, amputation, and death. The metabolic abnormalities caused by diabetes induce vascular dysfunction that predisposes this patient population to atherosclerosis. Blood pressure control, lipid-lowering therapy, angiotensin-converting enzyme inhibition, and antiplatelet drugs significantly reduce the risk of cardiovascular events. Although diabetic patients undergo revascularization procedures because of acute coronary syndromes or critical limb ischemia, the outcomes are less favorable than in nondiabetic cohorts. CONCLUSIONS: Since most patients with diabetes die from complications of atherosclerosis, they should receive intensive preventive interventions proven to reduce their cardiovascular risk.  相似文献   

16.
孙学玉  张芳  王修卫 《医学综述》2007,13(24):1990-1992
动脉粥样硬化是一种炎性疾病,炎症影响动脉粥样硬化斑块的稳定性和自然进程,C-反应蛋白是炎症的标志物。研究显示高敏C-反应蛋白是心血管新的危险因子,与急性冠状动脉综合征有良好的相关性。应用高敏C-反应蛋白预测急性冠状动脉事件具有较高的敏感性和精确性。干预高敏C-反应蛋白可以预防急性冠状动脉不良事件的发生。  相似文献   

17.
辛伐他汀对急性冠脉综合症患者单核细胞CX3CR1表达的影响   总被引:1,自引:0,他引:1  
目的 观察辛伐他汀对CX3CR1表达的影响,探讨他汀类药物可能的非调脂抗动脉粥样硬化作用.方法 63例冠状动脉造影确诊为急性冠脉综合征的患者按照处理因素不同分为对照组、10-7~10-5mol/L辛伐他汀不同浓度组和作用4、8、12 h不同时间组,用荧光定量RT-PCR技术检测各组患者中外周血单核细胞CX3CR1的表达情况.结果 不同浓度组中CX3CR1的表达均低于正常对照组(P<0.05),不同作用时间组中CX3CR1的表达均低于正常对照组(P<0.01).结论 辛伐他汀可降低CX3CR1的表达且呈浓度和时间依赖性,从而发挥抗炎及稳定斑块的作用.  相似文献   

18.
Inflammation, which plays a critical role in atherosclerosis and the occurrence of acute cardiovascular events, may be a new target for treatment of coronary artery disease(CAD) to reduce residual cardiovascular risk. Recently, Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease(CANTOS), the largest scale clinical trial that targeted inflammation but not lipids, has affirmed for the first time the inflammatory hypothesis of artherosclerosis and marked the advent of an exciting era of targeting inflammation for the prevention and treatment of cardiovascular diseases. Chinese medicine(CM) is a promising adjuvant therapy for CAD in light of its safety and pleiotropic effect of anti-inflammation, anti-platelet, lipid-regulating, endothelium-protection, microcirculation-improving, etc. In recent years, exploration of anti-inflammatory treatment of CAD with CM has been going on from theory to practice. Taking CANTOS as an example, the design strategy to combine CM and Western medicine to inhibit inflammation were discussed in this paper, which might provide a new perspective for CM intervention on CAD.  相似文献   

19.
目的 观察急性冠状动脉综合征患者血沉 (ESR)和C -反应蛋白 (CRP)阳性率 ,推断炎症反应在急性冠脉事件中的作用 ,及抗炎治疗对其影响。方法 测定 5 8例急性冠脉综合征患者的ESR和CRP阳性率 ,并与对照组进行比较。再分为抗炎组 ,非抗炎组 ,于治疗 1周后复查ESR和CRP ,进行治疗前后比较。结果 急性冠脉综合征患者ESR和CRP阳性率明显增高 ,抗炎后下降较明显。结论 作为炎症标记物 ,ESR值、CRP阳性率可作为预测因子 ,抗炎治疗在急性冠脉事件中可能是有益的  相似文献   

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