Angiopoietin-like protein 1 decreases blood brain barrier damage and edema following focal cerebral ischemia in mice

2008 ◽  
Vol 52 (3) ◽  
pp. 470-477 ◽  
Author(s):  
Dar-Ming Lai ◽  
Hung Li ◽  
Chin-Cheng Lee ◽  
Yi-Shiuan Tzeng ◽  
Yu-Hsuan Hsieh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Hyperbaric oxygen reduces blood-brain barrier damage and edema after transient focal cerebral ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S266-S266
Author(s):  
Roland Veltkamp ◽  
Li Sun ◽  
Dirk A Siebing ◽  
Katja Bieber ◽  
Sabine Heiland ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Hyperbaric Oxygen ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Transient Focal Cerebral Ischemia ◽  
Blood Brain Barrier Damage

Erythropoietin Prevents Blood Brain Barrier Damage Induced by Focal Cerebral Ischemia in Mice

2007 ◽  
Vol 32 (12) ◽  
pp. 2132-2141 ◽  
Author(s):  
Ying Li ◽  
Zhong-Yang Lu ◽  
Molly Ogle ◽  
Ling Wei
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

scholarly journals Description of a Novel Phosphodiesterase (PDE)-3 Inhibitor Protecting Mice From Ischemic Stroke Independent From Platelet Function

Stroke ◽  
2019 ◽  
Vol 50 (2) ◽  
pp. 478-486 ◽  
Author(s):  
Michael Bieber ◽  
Michael K. Schuhmann ◽  
Julia Volz ◽  
Gangasani Jagadeesh Kumar ◽  
Jayathirtha Rao Vaidya ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Platelet Function ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Local Inflammatory Response ◽  
Blood Brain ◽  
Blood Brain Barrier Damage

Background and Purpose— Acetylsalicylic acid and clopidogrel are the 2 main antithrombotic drugs for secondary prevention in patients with ischemic stroke (IS) without indication for anticoagulation. Because of their limited efficacy and potential side effects, novel antiplatelet agents are urgently needed. Cilostazol, a specific phosphodiesterase (PDE)-3 inhibitor, protected from IS in clinical studies comprising mainly Asian populations. Nevertheless, the detailed mechanistic role of PDE-3 inhibitors in IS pathophysiology is hardly understood. In this project, we analyzed the efficacy and pathophysiologic mechanisms of a novel and only recently described PDE-3 inhibitor (substance V) in a mouse model of focal cerebral ischemia. Methods— Focal cerebral ischemia was induced by transient middle cerebral artery occlusion in 6- to 8-week-old male C57Bl/6 wild-type mice receiving substance V or vehicle 1 hour after ischemia induction. Infarct volumes and functional outcomes were assessed between day 1 and day 7, and findings were validated by magnetic resonance imaging. Blood-brain barrier damage, as well as the extent of local inflammatory response and cell death, was determined. Results— Inhibition of PDE-3 by pharmacological blockade with substance V significantly reduced infarct volumes and improved neurological outcome on day 1 and 7 after experimental cerebral ischemia. Reduced blood-brain barrier damage, attenuated brain tissue inflammation, and decreased local cell death could be identified as potential mechanisms. PDE-3 inhibitor treatment did neither increase the number of intracerebral hemorrhages nor affect platelet function. Conclusions— The novel PDE-3 inhibitor substance V protected mice from IS independent from platelet function. Pharmaceutical inactivation of PDE-3 might become a promising therapeutic approach to combat IS via inhibition of thromboinflammatory mechanisms and stabilization of the blood-brain barrier.

scholarly journals Matrix Metalloproteinase-12 Induces Blood–Brain Barrier Damage After Focal Cerebral Ischemia

Stroke ◽  
2015 ◽  
Vol 46 (12) ◽  
pp. 3523-3531 ◽  
Author(s):  
Bharath Chelluboina ◽  
Jeffrey D. Klopfenstein ◽  
David M. Pinson ◽  
David Z. Wang ◽  
Raghu Vemuganti ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Matrix Metalloproteinase ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Blood Brain Barrier Damage ◽  
Matrix Metalloproteinase 12

scholarly journals Hyperbaric Oxygen Reduces Blood–Brain Barrier Damage and Edema After Transient Focal Cerebral Ischemia

Stroke ◽  
2005 ◽  
Vol 36 (8) ◽  
pp. 1679-1683 ◽  
Author(s):  
Roland Veltkamp ◽  
Dirk A. Siebing ◽  
Li Sun ◽  
Sabine Heiland ◽  
Katja Bieber ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Hyperbaric Oxygen ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Transient Focal Cerebral Ischemia ◽  
Blood Brain Barrier Damage

scholarly journals Early Appearance of Activated Matrix Metalloproteinase-9 after Focal Cerebral Ischemia in Mice: A Possible Role in Blood—Brain Barrier Dysfunction

1999 ◽  
Vol 19 (9) ◽  
pp. 1020-1028 ◽  
Author(s):  
Yvan Gasche ◽  
Miki Fujimura ◽  
Yuiko Morita-Fujimura ◽  
Jean-Christophe Copin ◽  
Makoto Kawase ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Vasogenic Edema ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Brain Barrier ◽  
Critical Event ◽  
Secondary Brain Injury ◽  
Blood Brain ◽  
Bbb Permeability

During cerebral ischemia blood–brain barrier (BBB) disruption is a critical event leading to vasogenic edema and secondary brain injury. Gelatinases A and B are matrix metalloproteinases (MMP) able to open the BBB. The current study analyzes by zymography the early gelatinases expression and activation during permanent ischemia in mice (n = 15). ProMMP-9 expression was significantly ( P < 0.001) increased in ischemic regions compared with corresponding contralateral regions after 2 hours of ischemia (mean 694.7 arbitrary units [AU], SD ± 238.4 versus mean 107.6 AU, SD ± 15.6) and remained elevated until 24 hours (mean 745,7 AU, SD ± 157.4). Moreover, activated MMP-9 was observed 4 hours after the initiation of ischemia. At the same time as the appearance of activated MMP-9, we detected by the Evan's blue extravasation method a clear increase of BBB permeability, Tissue inhibitor of metalloproteinase-1 was not modified during permanent ischemia at any time. The ProMMP-2 was significantly ( P < 0.05) increased only after 24 hours of permanent ischemia (mean 213.2 AU, SD ± 60.6 versus mean 94.6 AU, SD ± 13.3), and no activated form was observed. The appearance of activated MMP-9 after 4 hours of ischemia in correlation with BBB permeability alterations suggests that MMP-9 may play an active role in early vasogenic edema development after stroke.

Effects of Inhibition of Nitric Oxide Synthase on Blood-Brain Barrier Transport in Focal Cerebral Ischemia

Pharmacology ◽  
1994 ◽  
Vol 48 (6) ◽  
pp. 367-373 ◽  
Author(s):  
Oak Za Chi ◽  
Hwu Meei Wei ◽  
Arabinda K. Sinha ◽  
Harvey R. Weiss
Keyword(s):  
Nitric Oxide ◽  
Cerebral Ischemia ◽  
Nitric Oxide Synthase ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Oxide Synthase

The blood–brain barrier is continuously open for several weeks following transient focal cerebral ischemia

Neuroscience ◽  
2008 ◽  
Vol 153 (1) ◽  
pp. 175-181 ◽  
Author(s):  
D. Strbian ◽  
A. Durukan ◽  
M. Pitkonen ◽  
I. Marinkovic ◽  
E. Tatlisumak ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Blood Brain Barrier ◽  
Focal Cerebral Ischemia ◽  
Brain Barrier ◽  
Blood Brain ◽  
Transient Focal Cerebral Ischemia
Sign in / Sign up

Export Citation Format

Share Document