Objective: To analyze the changes and clinical significance of IL-6 and sICAM-1, and to explore their pathologic mechanism in the brain ischemia.
Methods: Thirty-two patients at Xiangya Hospital who experienced infarcts that occurred within the first 3 days were consecutively selected into the study, and 30 healthy subjects were selected as controls. The serum level of IL-6 and sICAM-1 was measured by radioimmunoassy and enzyme linked immunosorbent assay. Eleven out of the 32 patients that experienced stroke within 24 hours were observed on the 1st, 3rd, and 6th day. The subsequent volume of brain lesion as a consequence of stroke was measured by CT within 48 - 72 hours after the onset.
Results: Both the serum levels of IL-6 and sICAM-1 were significantly higher in patients within the first 3 days after the onset than those of the controls [(352. 1 +/- 31.7) pg/ml vs. (135.4 +/- 18.3) pg/ml, and (363.6 +/- 48.4) ng/ml vs. (227.2 +/- 30.1) ng/ml, P < 0.01]. The levels of IL-6 at the 6th day [(308.3 +/- 26.8) pg/ml] was significantly lower than that both on the 1st day [(364.5 +/- 29.7) pg/ml] and on the 3rd day [(345 +/- 28.9) pg/ml] (P <0.01). There was no significant difference between the 1st day and the 3rd day (P > 0.05). Statistical significance existed in each two concentrations of sICAM-1 on the 1st day [(383.9 +/- 56.1) ng/ml], the 3rd day [(354.6 +/- 40.8) ng/ml], and the 6th day [(316.7 +/- 32.3) ng/ml] (P < 0.05). Both the levels of IL-6 and sICAM-1 were higher in patients within the 6th day after the onset than those of sICAM-1 on the controls (P < 0.01). There was a positive correlation between both the levels of IL-6 and sICAM-1 at the first 3 days after the onset and the infarct volume (r = 0. 368, P < 0. 05 and r = 0. 594, P < 0. 01) , and the sICAM-1 positively correlated with IL-6 (r = 0. 453, P < 0. 05).
Conclusion: The serum levels of IL-6 and sICAM-1 were upregulated, which might play a role in inflammatory lesion, and the upregulation of sICAM-1 may be related to the IL-6. The levels of IL-6 and sICAM-1 may reflect both the degree of pathologic lesion after the brain ischemia and the infarct volume.