Serial Measurement Of Anti-inflammation Cytokines Interleukin-10 And Inflammatory Interleukin-8 In Serum Of Acute Cerebral Infarction And Associational Clinical Analysis

Objective: 1.To further reveal Interleukin-10(IL-10) and Interleukin-8(IL-8) participate in the pathophysiological process and its dynamical change rule by serially measuring the levels of IL-10 and IL-8 after acute cerebral infarction(ACI). 2. Further explore the correlation between brain damage and inflammation, and study the brain injury mechanisms after ACI. 3. To research the correlation between IL-10 and IL-8 ,including the severity and the volume of ACI, may help us to find new ways and methods for the prevention and treatment of ACI.Methods: 1. CI group: 30 cases fulfilled the select and exclude criteria: hospitalized within 24 hours, coincidence the criteria specified in the fourth cerebrovascular disease National Academic Conference diagnostic criteria and in confirmation of Computed Tomography(CT) and/or Magnetic Resonance Angiography(MRI),exclude such as acute and chronic inflammatory diseases(as severe upper respiratory tract infection, pneumonia, urinary system infection, hyperpyrexia et al ) before two weeks in hospital or during adopting blood , tumors, autoimmune disease,myocardial infarction,liver,kidney and endocrin diseases, peripheral vessels embolism diseases ,especial treatmeat in a month (Radiotherapy, Chemotherapy,Operation,using Biol praeparatum et al),stroke caused in three monthes ,lacunar infarction et al. Male:18, famale: 12, aged from 32 to 80, the average age 58.37±9.88 ; 30 age-matched health subjects as control group, male: 19, female: 11, aged from 34 to 77, Average 52.93±11.82. 2. Adopted elbow vein blood 3ml at days of 1, 3, 7, and 14. Serum samples were frozen in aliquots at -20℃within 2h of collection and avoided repeating to freeze and thaw. Control samples only adopted once and storage in the same conditions. 3.Levels of IL-10 and IL-8 were determined by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA). 4. Calculated methods of volumes:π/6 x long x width x high(cm3); 5. Neurological status was evaluated using the Glasgow Coma Scale and National Institutes of Health Stroke Scale. 6. Statistical evaluation was done using SAS6.12 statistical analysis software. All data were reported as mean±SD, Descriptive data of continuous variables were tested by Student t-test and analysis of variance and sum of ranks. Relevant analysis used spearman rank correlation. p<0.05 was considered statistically sighnificant.Results: 1.Dynamical expression of IL-10 was significantly increased in acute CI patients at each time points compared with controls. The level of IL-10 began to increase in the first 24 hours after ACI. Highest expression occurred at day 3, and it remained elevated at day 14 after CI (p<0.01). 2. Expression of IL-8 has the similar change .But Highest expression occurred at day 7, and it only remained elevated at day 1,3,and 7 after CI compared with controls(p<0.01).3. Expression of IL-10 did not correlate with the volume of ACI: large volume group (n=17, 16.61士5.32 pg/mL), small volume group (n=11, 16.51士5.60pg/mL), p>0.05. There are no correlation with IL-8 (r=0.2710, p>0.05), GCS scores(r=-0.3116, p>0.05) and NIHSS scores (r=0.3432, p>0.05). Serum IL-8 content correlated with the volume of ACI (r=0.4882, p<0.01), WBC(r=0.4575, p<0.05), not correlated with GCS scores (r=-0.1366, p>0.05) and NIHSS scores (r=0.1196, p>0.05).4. Highest NIHSS score of ACI occurred at day 3.there was statistical significantly in ACI patients compared with NIHSS scores at day 14(p<0.01)),not at day 1 and 7 ( p>0.05).Conclusion: IL-10 and IL-8 showed the dramatic change in serum of acute CI patients, it indicated IL-10 and IL-8 involved in the pathophysiological process. Serum IL-10 and IL-8 contents were correlated with the volume of CI, that mean they may participate in the formation of edema. Expression of IL-10 increased before the peak of edema. So we hypothesized Il-10 play a neuroprotective role after CI early onset, in coordination with inflammatory cytokine involved in brain edema formation. It is necessary to further investigate its role in CI and its correlation with inflammation, which may provide themry evidence to how lessening cerebral edema and reasonably use IL-10 in therapy of CI.