Assessment of Acute Phase Proteins in Acute Ischemic Stroke

Tamam, Yusuf; İltümür, Kenan; Apak, İsmail

doi:10.1620/tjem.206.91

Cited by 37 publications

(33 citation statements)

References 25 publications

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“…TMZ also limits membrane damage induced by reactive oxygen species (ROS) and protects tissue from free radicals with its antioxidant effects (Guarnieri and Muscari 1993;Doehner 1999;Tikhaze et al 2000;Kaminski et al 2002). It has been suggested that ROS-and nitric oxide (NO)-mediated damage enhances the release of proinflammatory mediators such as C-reactive protein (CRP), tumor necrosis factor-α (TNF-α ), interleukin-1 (IL-1) and IL-8 from macrophages both in inflammation and ischemia (Camussi et al 1991;Seo et al 1995;Halliwil et al 2000;Kuralay et al 2003;Tamam et al 2005).…”

confidence: 99%

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Kuralay

Altekin

Yazlar

et al. 2006

Tohoku J. Exp. Med.

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Percutaneous transluminal coronary angioplasty (PTCA) has been recognized as a reliable treatment procedure for acute reversible ischemia and reperfusion. Ischemic reperfusion cycle in PTCA leads to the systemic inflammation and extensive tissue injury by the production of reactive oxygen species including nitric oxide (NO) radicals. In patients with coronary artery disease, undergoing PTCA, the effects of trimetazidine (TMZ), a piperazine-derivative anti-anginal drug, were studied on several indirect markers of systemic inflammatory response: tumor necrosis factor-α (TNF-α ), C-reactive protein (CRP) and NO products (nitrite and nitrate). Patients (n = 11 each group) were untreated or pre-treated with TMZ (20 mg per orally three times a day), begun three days prior to PTCA, and marker levels were measured before the start of TMZ therapy (baseline), just before PTCA (0 hr), and 4, 24, and 48 hrs after PTCA. The baseline levels of markers were not significantly different between the untreated and pre-treated patients. In contrast, all parameters were lower in the TMZtreated group than those in the matched control group in the pre-and post-angioplasty periods. Interestingly, in the TMZ group, CRP and nitrite levels were significantly lower than in the control group at each time point of the pre-and post-angioplasty periods, but the TNF-α levels were significantly decreased only in the post-angioplasty period. Preprocedural treatment with oral TMZ for three days significantly suppressed the elevation of inflammatory markers before and shortly after PTCA. We suggest the usefulness of TMZ in preventing inflammatory cardiovascular events after PTCA.trimetazidine; percutaneous transluminal coronary angioplasty; C-reactive protein; nitric oxide; tumor necrosis factor-α .

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confidence: 99%

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Kuralay

Altekin

Yazlar

et al. 2006

Tohoku J. Exp. Med.

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“…The restoration of blood flow to the area surrounding the infarct elicits an inflammatory response that plays a significant role in secondary injury (1,2). The mechanisms associated with the initiation and perpetuation of inflammation are incompletely understood, but evidence from clinical and animal studies has implicated the complement system in postischemic cerebral injury (3,4). Mice deficient in C1q (blocked in the classical pathway of complement activation) have improved neurological outcome following the induction of cerebral ischemia, although the data proved difficult to interpret because C1q deficiency conferred significant protection only in neonatal mice (5,6).…”

mentioning

confidence: 99%

“…C1 inhibitor, however, was shown to be effective at reducing cerebral infarct volume in mature rodents (6 -8). Soluble complement receptor (CR) 3 1 (sCR1) has also been shown to be protective in a mouse model of ischemic stroke (9), although it was without significant effect in a neonatal rat model (10). P-selectin is an important mediator of platelet accumulation and neutrophil recruitment, and P-selectin expression is up-regulated in vitro by complement activation products (11,12).…”

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confidence: 99%

Complement-Dependent P-Selectin Expression and Injury following Ischemic Stroke

Atkinson¹,

Zhu

Qiao³

et al. 2006

The Journal of Immunology

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The mechanisms that contribute to inflammatory damage following ischemic stroke are poorly characterized, but studies indicate a role for both complement and P-selectin. In this study, we show that compared with wild-type mice, C3-deficient mice showed significant improvement in survival, neurological deficit, and infarct size at 24 h after middle cerebral artery occlusion and reperfusion. Furthermore, P-selectin protein expression was undetectable in the cerebral microvasculature of C3-deficient mice following reperfusion, and there was reduced neutrophil influx, reduced microthrombus formation, and increased blood flow postreperfusion in C3-deficient mice. We further investigated the use of a novel complement inhibitory protein in a therapeutic paradigm. Complement receptor 2 (CR2)-Crry inhibits complement activation at the C3 stage and targets to sites of complement activation. Treatment of normal mice with CR2-Crry at 30 min postreperfusion resulted in a similar level of protection to that seen in C3-deficient mice in all of the above-measured parameters. The data demonstrate an important role for complement in cerebrovascular thrombosis, inflammation, and injury following ischemic stroke. P-selectin expression in the cerebrovasculature, which is also implicated in cerebral ischemia and reperfusion injury, was shown to be distal to and dependent on complement activation. Data also show that a CR2-targeted approach of complement inhibition provides appropriate bioavailability in cerebral injury to enable complement inhibition at a dose that does not significantly affect systemic levels of serum complement activity, a potential benefit for stroke patients where immunosuppression would be undesirable due to significantly increased susceptibility to lung infection.

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“…Evidence has been accumulated from several prospective studies that high levels of high-sensitivity CRP (hsCRP) and fibrinogen were associated with elevated risk of coronary, cerebral and peripheral vascular disease (Danesh et al 1999;Maresca et al 1999;Tamam et al 2005).…”

mentioning

confidence: 99%

Association of C-Reactive Protein with the Presence and Extent of Angiographically Verified Coronary Artery Disease

Memon

Spasojević‐Kalimanovska

Bogavac-Stanojević

et al. 2006

Tohoku J. Exp. Med.

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Prospective studies have demonstrated that markers of inflammation, such as high-sensitivity C-reactive protein (hsCRP) and fibrinogen, predict future cardiovascular disease risk. However, the association between the hsCRP and fibrinogen levels and the extent of coronary stenosis in patients with coronary artery disease (CAD) remains controversial. The aim of our casecontrol study was to assess the association of inflammatory markers with the occurrence and extent of CAD. Serum hsCRP and plasma fibrinogen levels were measured in 138 patients with angiographically assessed CAD and in 183 healthy subjects matched according to age and gender. According to the number of significantly stenosed ( 50%) vessels, the patients were classified in four groups: those without stenosis (0-vessel disease) and those with 1, 2 or 3-vessel disease. The hsCRP and fibrinogen levels were significantly higher in patients than in controls ( p < 0.001). Although the hsCRP and fibrinogen levels tended to increase with the number of stenotic vessels, the differences were only significant for hsCRP ( p < 0.01). Regression analysis indicated hsCRP as an independent predictor for the presence (OR = 3.573, p < 0.05) and extent of CAD (β = 1.095, p < 0.05). In conclusion, the present study is the first report concerning the frequency distribution of hsCRP in Serbian healthy subjects and CAD patients. We have shown that elevated levels of hsCRP are associated with the presence and extent of CAD.atherosclerosis; inflammation; fibrinogen; hsCRP; coronary artery disease

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Assessment of Acute Phase Proteins in Acute Ischemic Stroke

Cited by 37 publications

References 25 publications

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Suppression of Angioplasty-Related Inflammation by Pre-Procedural Treatment with Trimetazidine

Complement-Dependent P-Selectin Expression and Injury following Ischemic Stroke

Association of C-Reactive Protein with the Presence and Extent of Angiographically Verified Coronary Artery Disease

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