interleukin-8 and Cerebral-Infarction

The present study aimed to explore the effects of edaravone on neurological function, tumor necrosis factor α (TNF-α), and interleukin (IL)-8 levels in patients with cerebral infarction.. A total of 96 patients with cerebral -infarction who were admitted to the department of neurology in our hospital were enrolled in the present study, and they were randomly assigned to Group A (n = 48) and Group B (n = 48). Group A was treated with conventional therapy plus edaravone for 2 weeks and Group B with conventional therapy alone for 2 weeks. Enzyme-linked immunosorbent assay was used to determine serum TNF-α and IL-8 levels before and after treatment, and Pearson correlation analysis was conducted to analyze the correlation between serum TNF-α and IL-8 levels as well as National Institutes of Health Stroke Scale (NIHSS) score.. After treatment, Group A had a lower NIHSS score and serum TNF-α and IL-8 levels as well as higher activities of daily living score than Group B (all p < 0.05). In addition, after treatment, no significant differences were observed between the 2 groups in terms of the presence of adverse reactions (p > 0.05). Pearson correlation analysis revealed a significant positive correlation between serum TNF-α and IL-8 levels as well as NIHSS score (r = -0.567 and r = -0.556, both p < 0.05).. Edaravone can improve the neurological function of patients without causing evident adverse reactions, thereby improving quality of life, which may be correlated to decreased serum TNF-α and IL-8 levels.

Topics: Activities of Daily Living; Aged; Cerebral Infarction; Edaravone; Female; Humans; Interleukin-8; Male; Middle Aged; Neuroprotective Agents; Recovery of Function; Treatment Outcome; Tumor Necrosis Factor-alpha

Progenitor cells (PCs) contribute to the endogenous repair mechanism after ischemic events. Interleukin-8 (IL-8) as part of the acute inflammatory reaction may enhance PC mobilization. Also, statins are supposed to alter number and function of circulating PCs. We aimed to investigate PC mobilization after acute ischemic stroke as well as its association with inflammatory markers and statin therapy. Sixty-five patients with ischemic stroke were enrolled in the study. The number of CD133+ PCs was analyzed by flow cytometry. Blood samples were drawn within 24 hours after symptom onset and after 5 days. The number of CD133+ PCs increased significantly within 5 days (p<0.001). We found no correlation between CD133+ PCs and the serum levels of IL-8, IL-6, or C-reactive protein (CRP). Multivariate analysis revealed that preexisting statin therapy correlated independently with the increase of CD133+ PCs (p=0.001). This study showed a mobilization of CD133+ PCs in patients with acute cerebral infarction within 5 days after symptom onset. The early systemic inflammatory response did not seem to be a decisive factor in the mobilization of PCs. Preexisting statin therapy was associated with the increase in CD133+ PCs, suggesting a potentially beneficial effect of statin therapy in patients with stroke.

Topics: AC133 Antigen; Acute Disease; Adult; Adult Stem Cells; Aged; Aged, 80 and over; Antigens, CD; Cerebral Infarction; Female; Glycoproteins; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Inflammation Mediators; Interleukin-6; Interleukin-8; Male; Middle Aged; Multivariate Analysis; Peptides; Phosphopyruvate Hydratase; Risk Factors; Young Adult

The aims of this study were to investigate the association between the +781C/T polymorphism of interleukin-8 (IL-8) and atherosclerotic cerebral infarction and the interaction between the +781C/T polymorphism and smoking or drinking in cerebral infarction in the Han Chinese population.. We investigated the +781C/T polymorphism of IL-8 in 308 consecutive Han Chinese patients who were diagnosed with atherosclerotic cerebral infarction and in 294 age- and gender-matched healthy control subjects. The patients were classified using the Oxfordshire Community Stroke Project (OCSP) classification. The patients and subjects' histories of smoking and drinking were recorded, and atherosclerosis (AS) of the internal carotid artery (ICA) was evaluated in the patients. The +781C/T polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP) analysis.. The +781C/T polymorphism and allele frequencies were not significantly different between the patients and controls and were not significantly associated with the OCSP classifications. We found that the 781C allele was significantly associated with AS of the ICA in the patients (p = 0.017), and the CT genotype was more prevalent in patients without AS of the ICA (p = 0.035). No interactions were observed between the +781C/T polymorphism and smoking or drinking.. Our results demonstrated that the +781C/T polymorphism of IL-8 did not play a role and had no interaction with smoking or drinking in the occurrence of cerebral infarction in the Han Chinese population. However, the C allele and the CT genotype might be associated with AS of the ICA in patients with ischemic stroke.

Topics: Aged; Alcohol Drinking; Cerebral Infarction; Female; Genetic Predisposition to Disease; Humans; Interleukin-8; Intracranial Arteriosclerosis; Male; Middle Aged; Polymorphism, Single Nucleotide; Smoking

The Korean genuine medicine "Seonghyangjeongkisan" (SHJKS) has long been used for various cerebrovascular diseases. However, very little scientific investigation has been carried out. Cytokines involved in the regulation of inflammatory reactions and immune responses may play a role in the pathogenesis of cerebral infarction (CI). The aim of the present study is to elucidate how SHJKS modulates the inflammatory reaction in lipopolysaccaride (LPS) plus phytohaemagglutinin (PHA)-stimulated peripheral mononuclear cells (PBMCs) from CI patients. The amount of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-6, and IL-8 in PBMC culture supernatant was significantly increased in the LPS plus PHA treated cells compared to unstimulated cells. SHJKS inhibited the TNF-alpha, IL-1beta, IL-6, and IL-8 production in dose dependent manner. Maximal inhibition rate of the TNF-alpha, IL-1beta, IL-6, and IL-8 by SHJGS (1.0 mg/ml) was 68.01 +/- 0.28% (P < 0.01), 52.11 +/- 0.56 % (P < 0.01), 53.42 +/- 0.46 % (P < 0.01), and 46.70 +/- 0.37% (P < 0.05), respectively. In addition, we show that SHJKS suppressed nuclear factor (NF)-kappaB activation induced by LPS plus PHA, leading to suppression of IkappaB-alpha phosphorylation and degradation. These results suggest that SHJKS might have regulatory effects on LPS plus PHA-induced cytokine production and NF-kappaB activation, which might explain its beneficial effect in the treatment of CI.

Topics: Aged; Anti-Inflammatory Agents; Biotransformation; Blotting, Western; Cell Nucleus; Cells, Cultured; Cerebral Infarction; Chromatography, High Pressure Liquid; Cytokines; Cytoplasm; Female; Humans; Indicators and Reagents; Interleukin-1beta; Interleukin-6; Interleukin-8; Lipopolysaccharides; Male; Middle Aged; Monocytes; NF-kappa B; Phytohemagglutinins; Plant Extracts; Tetrazolium Salts; Thiazoles; Tumor Necrosis Factor-alpha

To study the effects of a spin trap agent and a CD18 antibody administered after stroke induction on intracerebral hemorrhaging. The drugs can prevent leukocyte adhesion.. A rabbit embolic stroke model that produces intracerebral hemorrhage was used.. A time course study showed that hemorrhaging was grossly apparent in approximately 50% of the subjects at 5 hours and in 75% at 24 hours after embolization. MDL 101,002, a spin trap agent, administered IV 5 minutes after embolization, significantly decreased the volume of hemorrhage. It also improved the behavior score relative to vehicle-treated rabbits. The CD18 antibody tended to decrease hemorrhage volume.. The beneficial effect of MDL 101,002 may be caused by inhibition of free radical injury to brain tissue, thereby protecting brain microvessel integrity. Acute therapy for intracerebral hemorrhage may be feasible.

Topics: Animals; Antibodies, Monoclonal; Brain; Brain Edema; CD18 Antigens; Cerebral Hemorrhage; Cerebral Infarction; Disease Models, Animal; Extravasation of Diagnostic and Therapeutic Materials; Interleukin-8; Intracranial Embolism; Isoquinolines; Nitrogen Oxides; Rabbits; Spin Labels

Reperfusion after a transient ischemia is a frequently encountered clinical condition that often causes greater tissue damage than persistent ischemia itself. Reperfusion to rabbit brain, after a transient focal ischemia, induced neutrophil infiltration and aggregation--neither of which were observed in rabbit brain rendered ischemic alone for the same time interval--thereby leading to severe brain edema and infarct. Brain tissue levels of interleukin-8 (IL-8), a potent neutrophil chemotactic cytokine (chemokine), increased significantly at 6 hours after reperfusion, but without a noticeable elevation of plasma IL-8 levels. Moreover, we detected IL-8 protein immunohistologically in the vascular wall and, to a lesser degree, in infiltrated neutrophils, suggesting a local production of IL-8 in reperfused brain tissues. Furthermore, a neutralizing anti-IL-8 antibody significantly reduced brain edema and infarct size in comparison to rabbits receiving a control antibody. These results implicate locally produced IL-8 as a pivotal mediator of cerebral reperfusion and suggest that IL-8 is a novel target for the intervention of this injury.

Topics: Animals; Antibodies, Monoclonal; Blood-Brain Barrier; Brain Edema; Cerebral Infarction; Female; Interleukin-8; Mice; Neutrophils; Rabbits; Reperfusion Injury