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1.
Role of inflammation in the progression of heart failure 总被引:3,自引:0,他引:3
Yndestad A Damås JK Øie E Ueland T Gullestad L Aukrust P 《Current cardiology reports》2007,9(3):236-241
Chronic heart failure (HF) is a disorder characterized in part by immune activation and inflammation. Thus, patients with HF have elevated levels of a number of inflammatory cytokines, both in the circulation and in the failing heart itself. Several mechanisms for this immune activation, which are not mutually exclusive, have been suggested, including neurohormonal activation, hemodynamic overload, and activation of the innate immune system secondary to cardiac stress. Importantly, experimental studies have shown that inflammatory cytokines such as tumor necrosis factor-alpha, interleukin-1b, and monocyte chemoattractant peptide-1 may contribute to the development and progression of HF by promoting myocardial hypertrophy, activating matrix metalloproteinases, provoking contractile dysfunction, and inducing apoptosis. However, inflammatory cytokines may also have adaptive and cardioprotective effects. This important aspect of cytokine biology must be kept in mind when designing new immunomodulatory treatment modalities in HF. 相似文献
2.
Mona Hedayat Mohammad Jafar Mahmoudi Noel R. Rose Nima Rezaei 《Heart failure reviews》2010,15(6):543-562
Increased circulating and intracardiac levels of proinflammatory cytokines have been associated with chronic heart failure.
Following an initial insult, the increased production of proinflammatory cytokines, including TNF-α, IL-6, IL-1, and IL-18,
jeopardizes the surrounding tissue through propagation of the inflammatory response and direct effects on the cardiac myocyte
structure and function. Cardiac myocyte hypertrophy, contractile dysfunction, cardiac myocyte apoptosis, and extracellular
matrix remodeling contribute enormously to the development and progression of chronic heart failure. Despite the identification
of efficacious pharmacological regimens and introduction of mechanical interventions, chronic heart failure remains among
the leading causes of mortality worldwide. To introduce novel therapeutic strategies that modulate the inflammatory response
in the context of the failing heart, it is of prime importance to determine the contributions of TNF-α, IL-6, IL-1, and IL-18
in mediating cardiac adaptive and maladaptive responses, as well as delineating their downstream intracellular signaling pathways
and their potential therapeutic implications. 相似文献
3.
Asthma is a unique form of chronic airway inflammation characterized by reversible airway obstruction, airway hyperresponsiveness
and the production of specific inflammatory mediators. Local activation of both immune and nonimmune cells in the lung triggers
the release of these immunomodulator molecules. Among them, tumor necrosis factor (TNF)-α, a multipotent pro-inflammatory
mediator, plays a critical role in immunoregulation of asthma by contributing to bronchopulmonary inflammation and airway
hyperresponsiveness. Blocking TNF-α activity has already shown outstanding efficacy in other chronic inflammatory diseases
including rheumatoid arthritis, Crohn’s disease, and psoriasis. The successful treatment of these other chronic inflammatory
diseases provides hope that TNF inhibitors may have application for the treatment of asthma. Recent developments in animal
models and clinical trials in patients with severe asthma provide strong support for the concept that blocking TNF-α activity
represents a new approach in asthma therapy. In this review, we address the multipotential role of TNF-α in asthma and the
efficacy and safety of TNF-α blocking agents in asthma. 相似文献
4.
Advances in adipose tissue biology over the past 10 years have led to an improved understanding of the mechanisms linking
obesity with the metabolic syndrome and other complications. Obesity is characterized by a chronic, systemic low-grade state
of inflammation. Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6),
and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type
2 diabetes and cardiovascular disease. It is now clear that the adipocyte is an active participant in the generation of the
inflammatory state in obesity. Adipocytes secrete a variety of cytokines, including IL-6 and TNF-α, that promote inflammation.
Moreover, recent studies suggest that obesity is associated with an increase in adipose tissue macrophages, which also participate
in the inflammatory process through the elaboration of cytokines. An improved understanding of the role of adipose tissue
in the activation of inflammatory pathways may suggest novel treatment and prevention strategies aimed at reducing obesity-associated
morbidities and mortality. 相似文献
5.
van Grevenstein WM Hofland LJ van Rossen ME van Koetsveld PM Jeekel J van Eijck CH 《Digestive diseases and sciences》2007,52(10):2775-2783
Surgical handling of the peritoneum causes an inflammatory reaction, during which a potentially lethal cocktail of active
mediators is produced, including cytokines and growth factors. The aim of this study was to investigate the effects of inflammatory
cytokines on the interaction between tumor and mesothelial cells. Tumor cell adhesion to a mesothelial monolayer was assessed
after preincubation of the mesothelium with interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α.
Preincubation of the mesothelial monolayer with IL-1β or TNF-α resulted in enhanced tumor cell adhesion of Caco2 and HT29
colon carcinoma cells. The amount of stimulation for the Caco2 cells was between 20% and 40% and for HT29 cells between 30%
and 70%. Blocking experiments with anti–IL-1β and anti–TNF-α resulted in significant inhibition of the cytokine-stimulated
tumor cell adhesion. The presented results prove that IL-1β and TNF-α are significant stimulating factors in tumor cell adhesion
in vitro and may therefore account for tumor recurrence to the peritoneum in vivo. 相似文献
6.
Pen-Yuan Lin Hsi-Che Shen Chien-Jen Chen Shu-En Wu Hsien-Li Kao Jen-Hung Huang Danny Ling Wang Shih-Chung Chen 《Journal of thrombosis and thrombolysis》2010,29(1):52-59
Carvedilol, a nonselective β-adrenoceptor antagonist, has been shown to possess antioxidant effects and reduce the risk of
hospitalization and death in patients with severe congestive heart failure, which is featured by the activation of pro-inflammatory
cytokines, including tumor necrosis factor-α (TNF-α), and leads to thrombotic complications. Thrombomodulin (TM) plays protective
roles against thrombosis. Treatment of ECs with TNF-α resulted in a down-regulation in the TM expression in a time-dependent
manner. Pre-treatment of ECs with carvedilol (1 and 10 μM) for 1 h significantly up-regulated the TM expression in ECs in
response to TNF-α. When ECs were pre-treated with a nuclear factor-κB (NF-κB) inhibitor, i.e., parthenolide, their TNF-α-mediated
down-regulation of TM expression was inhibited. Pre-treatment of ECs with carvedilol inhibited the NF-κB-DNA binding activity
in ECs induced by TNF-α. Our findings provide insights into the mechanisms by which carvedilol exerts anti-thrombotic effects
by inducing TM expression in ECs in response to pro-inflammatory stimulation. 相似文献
7.
Heart failure (HF) is characterized by the elaboration of a portfolio of pro-inflammatory cytokines and inflammatory mediators
that are considered to contribute to disease progression by virtue of the deleterious effects that these molecules exert on
the heart and circulation. Recent studies have suggested that these inflammatory mediators may serve as relevant markers of
disease severity and HF prognosis. Moreover, there is evidence that changes in the levels of inflammatory biomarkers may prove
useful in following the change in patient clinical status following institution of appropriate HF therapy. This review will
focus on the emerging role of inflammatory biomarkers, including pro-inflammatory cytokines, C-reactive protein, and erythrocyte
sedimentation rate in patients with HF. 相似文献
8.
There is an emerging interest in the role of anti-TNF-α therapy in reducing bone damage in chronic arthritis with special
regard to rheumatoid arthritis. Accumulation of osteoclasts in rheumatoid synovial tissues, and their activation due to osteoclastogenic
cytokines and chemokines at cartilage erosion sites suggest that they may advantageously be considered as therapeutic targets.
Given that the primary role of TNF-α in osteoclastogenesis, the inhibition of TNF-α represents an important strategy for reducing
bone damage in rheumatoid arthritis. In point of fact, there is evidence that treatment with anti-TNF-α agents may avoid or
reduce bone damage in rheumatoid arthritis, even if further studies are required to provide a biological explanation and a
link for the observation of the advantageous effects of TNF-α inhibitors on the progression of bone damage in chronic arthritis.
The existence of factors involved in osteoclast activation, including IL-1, IL-6, IL-7, IL-11, IL-17, M-CSF, TGF-β, MIP-1α,
MIP-1β, IP-10, MIG, and OSCAR, indicates that TNF-α is only a single player in the great molecular cauldron of osteoclastogenesis.
The presence of mediators behind the TNF-α and RANK-RANKL complex that may be independent in inducing osteoclastogenesis,
such as NFATc1, suggests that the anti-TNF-α therapy will not provide a complete reduction of bone damage in chronic arthritis. 相似文献
9.
Tumor necrosis factor-alpha is expressed by monocytes/macrophages following cardiac microembolization and is antagonized by cyclosporine 总被引:7,自引:0,他引:7
M. Arras R. Strasser M. Mohri R. Doll P. Eckert W. Schaper J. Schaper 《Basic research in cardiology》1998,93(2):97-107
The time course of expression of TNF-α in myocardial wound healing following ischemic injury was investigated in the porcine
heart. Microembolization was used to induce focal ischemia and necrosis in hearts of 39 adult pigs. The animals were sacrified
after 3, 6, 12, 24 h, 3 and 7 days, and after 4 weeks, and the myocardial tissue was studied by immunofluorescence using specific
antibodies. TNF-α containing cells were identified as monocytes/macrophages by double staining with a muramidase antibody.
Monocytes/macrophages were the only source of TNF-α. Microembolization caused multiple necrotic foci with loss of myocytes
in the left ventricular myocardium. These foci contained numerous monocytes/macrophages and showed an inflammatory reaction
typical of wound healing followed by replacement with scar tissue. The number of TNF-α positive cells increased after 24 h,
peaked between 3–7 days and slowly decreased thereafter. Expression of TNF-α in monocytes/macrophages was significantly reduced
after pretreatment of pigs with cyclosporine or dexamethasone. It is concluded that 1.) in myocardial tissue monocytes/macrophages
are the only cell type expressing TNF-α, 2.) TNF-α is involved in wound healing after ischemia, and 3.) synthesis of TNF-α
and inflammatory angiogenesis can be inhibited be treatment with either cyclosporine or dexamethasone.
Received: 23 June 1997, Returned for revision: 20 August 1997, Revision received: 10 December 1997, Accepted: 17 January 1998 相似文献
10.
Richard P. MacDermoit 《Journal of gastroenterology》1996,31(6):907-916
The normal intestinal immune system is under a balance in which proinflammatory and anti-inflammatory cells and molecules
are carefully regulated to promote a normal host mucosal defense capability without destruction of intestinal tissue. Once
this careful regulatory balance is disturbed, nonspecific stimulation and activation can lead to increased amounts of potent
destructive immunologic and inflammatory molecules being produced and released. The concept of balance and regulation of normal
mucosal immune and inflammatory events is indicative of how close the intestine is to developing severe inflammation. The
normal intestinal mucosal immune system is constantly stimulated by lumenal contents and bacteria. The stimulatory molecules
present in the intestinal lumen that activate and induce subsequent mucosal immunologic and inflammatory events include bacterial
cell wall products, such as peptidoglycans and lipopolysaccharides, as well as other chemotactic and toxic bacterial products
that are produced by the many different types of bacteria within the gastrointestinal tract. These highly stimulatory bacterial
cell wall products are capable of activating macrophages and T lymphocytes to release potent proinflammatory cytokines, including
interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α). IL-1, IL-6, and TNF-α increase the presence
of human leukocyte antigen (HLA) class II antigen-presenting molecules on the surfaces of epithelial cells, endothelial cells,
macrophages, and B cells, thus increasing their ability to present lumenal antigens and bacterial products. The proinflammatory
cytokines IL-1 and TNF-α also increase the ability of epithelial cells, endothelial cells, macrophages, and fibroblasts to
secrete potent chemotactic cytokines, such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1), which serve
to increase the movement of macrophages and granulocytes from the circulation into the inflamed mucosa. Thus, through lumenal
exposure to potent, nonspecific stimulatory bacterial products, the state of activation of the intestinal immune system and
mucosal inflammatory pathways are markedly up-regulated. This raises the question of whether there is a deficiency in effective
down-regulation through the absence of normally suppressive cytokines such as interleukin-10 (IL-10), transforming growth
factor-β (TGF-β), interleukin-4 (IL-4), and IL-1 receptor antagonist. Normally, the turning off of the active and destructive
immunologic and inflammatory events should occur following the resolution of a bacterial or viral infection that has been
appropriately defended against and controlled by the mucosal immune system. In inflammatory bowel disease (IBD), however,
the down-regulatory events and processes that should turn off the immunologic and inflammatory protective processes, once
the pathogenic agent has been cleared, appear to be deficient or only partially effective. We may find that we ultimately
are dealing with disease processes that have more than one genetic or cellular basis. The improved understanding of the immunopathophysiology
of IBD will allow exploration of novel immunologic and genetic approaches, such as gene replacement therapy, administration
of a suppressor cytokine or an altered cell surface antigen, the administration ofhumanized monoclonal antibodies directed against proinflammatory cytokines, or the development of newer strategies against fundamenial
cell biologic mechanisms such as adhesion molecules. 相似文献
11.
Evidence from both experimental and clinical trials indicates that inflammatory mediators are of importance in the pathogenesis of chronic heart failure (HF) contributing to cardiac remodeling and peripheral vascular disturbances. Several studies have shown raised levels of inflammatory cytokines such as tumor necrosis factor (TNF)α, interleukin (IL)-1β and IL-6 in HF patients in plasma and circulating leukocytes, as well as in the failing myocardium itself. There is strong evidence that these mediators are involved in processes leading to cardiac remodeling such as hypertrophy, fibrosis and apoptosis. Some of these cytokines can also give useful prognostic information as reliable biomarkers in this disorder. In general, immunomodulating treatments have, with a few exceptions, been neutral or even harmful. However, the negative results of anti-TNF studies, for instance, do not necessarily argue against the 'cytokine hypothesis'. These studies just underscore the challenges in developing treatment modalities that can modulate the cytokine network in HF patients and result in beneficial net effects. Future studies should identify the crucial actors and their mechanisms of action in the immunopathogenesis of chronic HF and, in particular, clarify the balance between adaptive and maladaptive effects of these molecules. Such studies are a prerequisite for the development of new treatment strategies that target inflammatory and immunopathogenic mechanisms in HF. In this review article, these issues are thoroughly discussed, and we also argue for the possibility of future therapeutic targets such as mediators in innate immunity, chemokines and mediators in matrix remodeling. 相似文献
12.
A variety of clinical and experimental investigations have suggested that tumor necrosis factor alpha (TNF-α) may play a role
in the pathophysiology of heart failure. Serum levels of TNF-α are elevated in patients with heart failure, and both cardiac
and infiltrating cells of the myocardium can produce this proinflammatory cytokine. Both cardiac myocytes and nonmyocytes
also express receptors for TNF-α, and experimental studies on isolated cells, muscles, and transgenic models demonstrate the
ability of TNF-α to recapitulate functional and biochemical alterations resembling that observed in human congestive heart
failure. The intracellular pathways affected by TNF-α include production of ceramide and an alteration in calcium metabolism.
Recent studies in both animal models and clinical investigations suggest that anti-TNF-α therapies may limit the pathophysiologic
consequences of congestive heart failure. 相似文献
13.
Yukihito Sato Yoshiki Takatsu Haruyasu Ito Kazuaki Kataoka Yuzou Takeuchi Akira Matsumori 《Heart and vessels》1996,11(4):218-220
Summary Elevated levels of circulating tumor necrosis factor (TNF)-α have been reported in patients with decreased left ventricular
ejection fraction. Also, TNF has been reported to depress myocardial contractility. In our previous study, no correlation
was found between the plasma level of TNF and clinical parameters in patients with cardiomyopathy. In the present study, we
detected elevated levels of circulating TNF-α in 5 out of 15 patients with mitral valve disease and in 1 patient with ventricular
septal defect whose left ventricular ejection fraction was within the normal range. The levels of TNF-α were not correlated
with any hemodynamic parameters. Further studies are necessary to clarify the mechanisms of the regulation and effects of
TNF-α in patients with chronic heart failure. 相似文献
14.
Niebauer J 《Heart failure reviews》2008,13(1):39-49
Cardiologists now recognize that the cardio-centric model of heart failure does not sufficiently explain the entire traits
particular to chronic heart failure. Evidence accumulates, that many features of the syndrome can be explained by the known
biological effects of inflammatory mediators. Indeed, when expressed in experimental models at concentrations commonly observed
in heart failure, inflammatory mediators such as tumor necrosis factor-α, interleukin-6, and nitric oxide can produce effects
that mimic features of heart failure, including (but not limited to) progressive left-ventricular dysfunction, pulmonary edema,
left-ventricular remodeling, and cardiomyopathy. As we witness anti-cytokine therapies and other strategies to avoid an increase
in cytokines we have been shown that acute bouts of exercise are associated with an increase in pro-inflammatory cytokines
and markers of oxidative stress. As a consequence we have been warned exercise may thus even further contribute to the deterioration
of heart failure. However, there are several randomized trials which unanimously document that chronic—as opposed to acute
bouts of—exercise does not only lead to a reduction of cytokines and oxidative stress, but that patients dramatically benefit
by the increase in maximal oxygen consumption, exercise capacity, quality of life, reduction in hospitalization, morbidity,
and mortality. Over the past two decades it has become evident that cytokine research has come to stay and that we will continue
to see anti-cytokine treatment strategies for our patients. It is the aim of this review to shed some more light on the most
commonly investigated and most relevant cytokines. 相似文献
15.
Akazawa A Sakaida I Higaki S Kubo Y Uchida K Okita K 《Journal of gastroenterology》2002,37(5):345-353
Background:
Background: Tumor necrosis factor-α (TNF-α), may be involved in the pathogenesis of inflammatory bowel diseases (IBDs). The aim of this
study was to evaluate the effect of TNF-α on the inflammatory activity of IBD.
Methods: TNF-α mRNA expression in intestinal mucosal biopsy specimens from IBD patients [ulcerative colitis (UC), n= 54; and Crohn's disease (CD), n= 11] was analyzed using a competitive polymerase chain reaction. The degree of macrophage infiltration was analyzed by immunohistochemistry,
using an anti-human CD68 antibody.
Results: TNF-α mRNA expression was increased in UC patients, corresponding to the inflammatory activity. However, in CD, TNF-α mRNA
expression was not correlated with the endoscopic findings.
Conclusions: We clarified that TNF-α mRNA expression was responsible for the inflammatory activity in UC. However, TNF-α mRNA expression
was not correlated with the mucosal injury in CD.
Received: February 9, 2001 / Accepted: September 28, 2001 相似文献
16.
The aim of this study is to investigate the induction of interleukin-34 (IL-34) and macrophage colony-stimulating factor (M-CSF)
mRNA by inflammatory cytokines and the involvement of mitogen-activated protein kinases (MAPKs) in this signaling pathway
in human osteoblasts as both IL-34 and M-CSF bind to the same receptor c-FMS. Among four inflammatory cytokines [(IL-1β, IL-6,
IL-17, and tumor necrosis factor-α (TNF-α)], IL-34 mRNA expression level was dramatically induced by IL-1β (17-fold) and TNF-α
(74-fold). IL-1β and TNF-α activated the intracellular mitogen-activated protein kinases (MAPKs): p44/42 MAPK, p38, and c-Jun
N-terminal kinase (JNK) as well as nuclear factor-κB (NF-κB) in osteoblasts. IL-1β- and TNF-α-mediated induction of IL-34
mRNA expression was decreased by JNK inhibitor. Interestingly, although treatment of MEK-1/2 inhibitor showed no reduction
in the increase of IL-34 mRNA expression by cytokines, combination of MEK-1/2 inhibitor and JNK inhibitor significantly inhibited
IL-1β- and TNF-α-mediated IL-34 mRNA expression level compared to those by each inhibitor alone. On the other hand, M-CSF
mRNA expression level was significantly induced by both IL-1β and TNF-α by up to 7- and 11-fold, respectively. IL-1β- and
TNF-α-mediated induction of M-CSF mRNA was not affected by p38, JNK, and MEK-1/2 inhibitors. However, NF-κB inhibitor completely
inhibited the elevation of M-CSF mRNA expression by these cytokines. These results showed that proinflammatory cytokines,
IL-1β and TNF-α, induced the expression of IL-34 mRNA via JNK and p44/42 MAPK but not p38 in human osteoblasts while p38,
JNK, and p44/42 MAPK were not involved in the induction of M-CSF mRNA expression by these cytokines. 相似文献
17.
Reduced uterine perfusion pressure during pregnancy is an important initiating event in preeclampsia. Inflammatory cytokines
are thought to link placental ischemia with cardiovascular and renal dysfunction. Supporting a role for cytokines are findings
of elevated tumor necrosis factor (TNF)-α and interleukin (IL)-6 plasma levels in preeclamptic women. Blood pressure regulatory
systems (eg, renin-angiotensin system [RAS] and sympathetic nervous system) interact with proinflammatory cytokines, which
affect angiogenic and endothelium-derived factors regulating endothelial function. Chronic reductions in placental perfusion
in pregnant rats are associated with enhanced TNF-α and IL-6 production. Chronic infusion of TNF-α or IL-6 into normal pregnant
rats significantly increases arterial pressure and impairs renal hemodynamics. TNF-α activates the endothelin system in placental,
renal, and vascular tissues, and IL-6 stimulates the RAS. These findings suggest that inflammatory cytokines elevate blood
pressure during pregnancy by activating multiple neurohumoral and endothelial factors. 相似文献
18.
19.
Ostör AJ 《Clinical rheumatology》2008,27(11):1343-1353
Rheumatoid arthritis (RA) is a debilitating autoimmune disease that has traditionally been treated with disease-modifying
anti-rheumatic drugs (DMARDs). In the European Union (EU), patients who fail to respond to traditional DMARDs may receive
tumor necrosis factor-α (TNF-α) antagonists. However, approximately one-third of patients fail TNF-α antagonists due to adverse
effects or lack of efficacy, and there are limited treatment options available to these patients. As knowledge of the underlying
immunopathology of RA evolves, new strategies for inhibiting the inflammatory process have emerged. It is well known that
activated T cells play a key role in orchestrating the immunopathological mechanisms of RA. Inhibiting the full activation
of T cells is a rational strategy in the treatment of RA and represents a novel method of inhibiting disease activity, distinct
from inflammatory cytokine blockade. Here, the safety and efficacy of abatacept, a selective T-cell co-stimulation modulator
recently approved in the EU, is reviewed in patients with RA who have shown an inadequate response to TNF-α antagonists. In
a randomized, placebo-controlled, double-blind, phase III trial of patients with an inadequate response to TNF-α antagonism,
abatacept was effective in improving the signs and symptoms of RA, as well as patient-centered outcomes, such as fatigue,
disability, and other mental and physical aspects of health-related quality of life. These improvements were sustained through
2 years during the open-label, long-term extension period. In this trial, abatacept demonstrated a safety and tolerability
profile similar to placebo. Taken together, these data suggest that selective co-stimulation modulation with abatacept may
be a viable option for patients who are refractory to both traditional therapies and TNF-α antagonists.
An erratum to this article can be found at 相似文献
20.
Effect of cilostazol, a selective type-III phosphodiesterase inhibitor, on water-immersion stress-induced gastric mucosal injury in rats 总被引:1,自引:0,他引:1
Ohba R Otaka M Odashima M Jin M Komatsu K Konishi N Wada I Horikawa Y Matsuhashi T Oyake J Hatakeyama N Watanabe S 《Journal of gastroenterology》2006,41(1):34-40
Background Cilostazol, a specific type-III phosphodiesterase inhibitor, is widely used for the treatment of ischemic symptoms of peripheral
vascular disease. Recent studies have reported that the mechanism of cilostazol is related to the suppression of pro-inflammatory
cytokine production and improvement of local microcirculation disturbances. The pathogenesis of stress-induced gastric mucosal
lesions is characterized by the activation of inflammatory cells and the production of inflammatory cytokines. The effects
of cilostazol on the development of gastric mucosal lesions have not been reported. In the present study, we examined the
effect of a cilostazol on water-immersion stress-induced gastric mucosal lesions.
Methods Rats were subjected to water-immersion stress with or without pretreatment with a single intraperitoneal injection of the
selective type-III phosphodiesterase inhibitor, cilostazol. We measured the gastric mucosal lesion and the concentrations
of myeloperoxidase (MPO), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and cytokine-induced neutrophil chemoattractant-1
(GRO/CINC-1), as an index of neutrophil accumulation and pro-inflammatory cytokine production.
Results Cilostazol ameliorated the gastric mucosal injury induced by water-immersion stress (P < 0.001). The gastric contents of MPO, TNF-α, IL-1β, and CRO/CINC-1 were all increased after water-immersion stress and were
reduced to almost normal levels by cilostazol.
Conclusions In this study, we demonstrated that a selective type-III phosphodiesterase inhibitor, cilostazol, inhibited stress-induced
gastric inflammation and damage via suppressing the production of pro-inflammatory cytokines. Cilostazol may be useful for
preventing gastric mucosal lesions. 相似文献