BACKGROUND: Activated leukocytes and their mediators may participate in ischemic brain injury. Secretory leukocyte protease inhibitor (SLPI) plays an important role in regulating the activity of the proteases, and may limit tissue damage. The aim of this study was to evaluate the changes in SLPI level in ischemic stroke patients. METHODS: The study comprised 20 patients with ischemic stroke and 20 controls. SLPI levels were measured in serum using enzyme-linked immunosorbent assay on the 1st, 5th and 12th day after stroke onset. RESULTS: SLPI was increased in the whole group of ischemic stroke patients compared with controls. It was also significantly increased on the 1st, 5th and 12th day after stroke in patients with larger brain tissue damage involving one or more lobe of the brain and in patients with more severe clinical status compared to controls (p < 0.05). A significant correlation between SLPI and the extent of brain tissue damage was observed on the 12th day after ischemic stroke onset (p < 0.05). CONCLUSIONS: Our results suggest that SLPI takes part in the anti-inflammatory reaction after ischemic stroke. Endogenous SLPI may have a neuroprotective effect, and could be a prototype therapeutic approach for ischemic stroke. Copyright 2002 S. Karger AG, Basel
BACKGROUND: Activated leukocytes and their mediators may participate in ischemic brain injury. Secretory leukocyte protease inhibitor (SLPI) plays an important role in regulating the activity of the proteases, and may limit tissue damage. The aim of this study was to evaluate the changes in SLPI level in ischemic strokepatients. METHODS: The study comprised 20 patients with ischemic stroke and 20 controls. SLPI levels were measured in serum using enzyme-linked immunosorbent assay on the 1st, 5th and 12th day after stroke onset. RESULTS:SLPI was increased in the whole group of ischemic strokepatients compared with controls. It was also significantly increased on the 1st, 5th and 12th day after stroke in patients with larger brain tissue damage involving one or more lobe of the brain and in patients with more severe clinical status compared to controls (p < 0.05). A significant correlation between SLPI and the extent of brain tissue damage was observed on the 12th day after ischemic stroke onset (p < 0.05). CONCLUSIONS: Our results suggest that SLPI takes part in the anti-inflammatory reaction after ischemic stroke. Endogenous SLPI may have a neuroprotective effect, and could be a prototype therapeutic approach for ischemic stroke. Copyright 2002 S. Karger AG, Basel
Authors: Cecilia Berardi; Christine L Wassel; Paul A Decker; Nicholas B Larson; Phillip S Kirsch; Mariza de Andrade; Michael Y Tsai; James S Pankow; Michele M Sale; Hugues Sicotte; Weihong Tang; Naomi Q Hanson; Mary M McDermott; Michael H Criqui; Michael A Allison; Suzette J Bielinski Journal: Angiology Date: 2016-07-20 Impact factor: 3.619
Authors: Sari S Hannila; Mustafa M Siddiq; Jason B Carmel; Jianwei Hou; Nagarathnamma Chaudhry; Peter M J Bradley; Melissa Hilaire; Erica L Richman; Ronald P Hart; Marie T Filbin Journal: J Neurosci Date: 2013-03-20 Impact factor: 6.167