The temporal profiles of ICAM-1 expression and leukocytes infiltration after focal cerebral ischemia/reperfusion
Wei Dong
Abstract
Wei Dong
Abstract
Objective To study the temproal course of expression of ICAM-1 protein and the feature of neutrophils infiltration in rat brain after MCA occlusion/reperfusion. Methods The animal models of the MCA ischemia/reperfusion was established in Wistar rats. The expression of ICAM 1 was measured by immunohistochemistry and the neurtrophil infiltration was determined by the evaluation of MPO. Results (1)ICAM 1 immunoractivity was enhanced in microvessels in the ischemic lesion at 6h after reperfusion,reached the peak at 36~48h,and then decreased gradually,but at the 7th day,upregulation of ICAM 1 expression still existed. (2)Neurons also expressed ICAM 1 at the border of infarct. (3)MPO activity rose at 6h,reached the peak at 24~36h and then returned to near normal level at 6d. Conclusion (1)Up regulation of ICAM-1 in microvessel occured after ischemia/reperfusion,it also existed in neurons at the border of infarct. (2)The feature of neutrophils infiltration in ischemic region had the similar regularity to expression of ICAM-1.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To study the temproal course of expression of ICAM-1 protein and the feature of neutrophils infiltration in rat brain after MCA occlusion/reperfusion. Methods The animal models of the MCA ischemia/reperfusion was established in Wistar rats. The expression of ICAM 1 was measured by immunohistochemistry and the neurtrophil infiltration was determined by the evaluation of MPO. Results (1)ICAM 1 immunoractivity was enhanced in microvessels in the ischemic lesion at 6h after reperfusion,reached the peak at 36~48h,and then decreased gradually,but at the 7th day,upregulation of ICAM 1 expression still existed. (2)Neurons also expressed ICAM 1 at the border of infarct. (3)MPO activity rose at 6h,reached the peak at 24~36h and then returned to near normal level at 6d. Conclusion (1)Up regulation of ICAM-1 in microvessel occured after ischemia/reperfusion,it also existed in neurons at the border of infarct. (2)The feature of neutrophils infiltration in ischemic region had the similar regularity to expression of ICAM-1.
Key concepts: Infiltration (HVAC), Ischemia, ICAM-1, Microvessel, Immunohistochemistry, Pathology, Medicine, Reperfusion injury