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  • CVT 10216 receptor br Inflammatory cytokines in ICH secondar


    Inflammatory cytokines in ICH secondary injury
    Strategies with potential translation from the laboratory to the clinic Inflammation is a dynamic process of injury and repair that responds to various stress and damage factors. Significant changes in cytokines associated with the basic inflammatory pathology occur in the ICH CVT 10216 receptor and may serve as new therapeutic targets (Chang et al., 2017, Lan et al., 2017b, Zhang et al., 2017). However, excessive inhibition of inflammation after ICH not only increases the risk of infection (Tapia-Perez et al., 2016), but also delays hematoma clearance and tissue repair (Zhang et al., 2017). Enhancement of overall inflammatory response will aggravate secondary brain injury after ICH (Zhou et al., 2014). Therefore, the key point of the therapeutic strategy is to regulate the balance of the proinflammatory and anti-inflammatory response in order to reduce brain damage and promote brain repair. This strategy can be achieved by increasing the anti-inflammatory cytokines and/or decreasing the proinflammatory cytokines. To date, research into the reduction of ICH injury by altering these cytokines has been conducted mostly in rodent models. Although these studies have focused on only a few cytokines, it is clear that the inhibition of proinflammatory cytokines or augmentation of CVT 10216 receptor anti-inflammatory cytokines can alleviate inflammatory reactions, reduce brain edema, increase stability of the BBB, reduce brain injury, and improve neurologic function (King et al., 2011, Lu et al., 2014, Masada et al., 2003, Mayne et al., 2001, Sinn et al., 2007, Yang et al., 2014). These animal studies are summarized in Table 2. Previous and ongoing clinical trials have been summarized in a recent review (Siaw-Debrah et al., 2017). To our knowledge, there are no ongoing or completed clinical trials focusing on cytokines in ICH. Published studies have focused mainly on cytokine changes in ICH patients (summarized in Table 3). The current challenge will be successful translation of preclinical experiments to clinical trials.
    Concluding remarks
    Introduction Heart diseases are theleading cause of mortality and morbidity in the developed world [1]. According to the European Heart Network, 47% of all deaths in Europe are caused by heart diseases [2] and according to the American Heart Association, prevalence of heart diseases will continue to increase. It is believed that by year 2030, more than 116 million people in United States will develop a form of heart disease [3]. The term heart disease includes a wide range of conditions that affect the heart function, the most notorious of which is atherosclerotic coronary disease caused by, atherosclerosis, a chronic inflammatory condition that is characterized by reduced blood flow through the coronary artery [4]. Atherosclerotic plaque builds up in the arterial wall causing occlusion of the vessel. While traditional therapeutic approaches for heart diseases include broad-spectrum angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, beta-adrenergic blocking agents etc., a modern approach focuses on designing drugs to inhibit specific mediators and cytokines in the inflammatory pathway. The therapeutic strategy of these drugs is to either block pro-inflammatory cytokines or facilitate delivery of anti-inflammatory cytokines [5].