Abstract TP65: Fas Ligand Induced Brain Inflammation After Ischemic Stroke And Attenuates By Human Urinary Kallidinogenase
Inflammation is an important contributing mechanism in ischemic stroke. Fas ligand plays a critical role in post-stroke inflammatory responses. However, little progress has been made in clinical therapy, especial the treatment of inflammation after ischemic stroke. From 2010-2012, acute brain infarction patients within 72 hours of onset in the territory of anterior circulation artery have been enrolled in this study. All the patients were randomized to the HUK treated group (HP) and non HUK treated group (control group, CP). Both two groups received the same foundation treatment. In HP group, the patients received an intravenous transfusion of HUK once a day, for 10 days. The NIHSS index were used to evaluate neurological deficit at both day 0, days 10 and day 90. All patients were imaged with 3.0T MRI at both day 0 and day 10. The ischemic lesion area was measured by both DWI, PWI and FLAIR. The brain edema extent were compared. The blood samples were taken by all the patients for sFAL and inflammation factors detection at day 0, day 10 and day 90. We found: 1) 206 patients were enrolled in this study, 117 patients were in HP group and 89 patients were in CP group. The NIHSS index and brain edema extent show no significant difference between the HP group and CP group at day 2) sFAL could be detected in peripheral blood, and the level of sFAL had an significant increase at day 10 compared to day 0. Both inflammation cells and inflammation factors were increased at day 10 as compared to day 0. 3) As patients which received the HUK treatment, we observed the obvious improvement of NIHSS score, brain edema as well as inflammatory mediators. sFAL induced inflammation might contribute to the brain injury after ischemic stroke, and HUK protects against ischemic brain injury by inhibiting inflammatory response.
- © 2012 by American Heart Association, Inc.