Intracerebral Hemorrhage in Mice.

Intracerebral hemorrhage is the most devastating stroke subtype with high rates of mortality and morbidity. Furthermore, no clinically approved treatment exists that effectively increases survival or improves quality of life for survivors. Effective modeling is necessary to elucidate the pathophysiological mechanisms of intracerebral hemorrhage and evaluate potential therapeutic approaches.

Adropin preserves the blood-brain barrier through a Notch1/Hes1 pathway after intracerebral hemorrhage in mice.

Adropin is expressed in the CNS and plays a crucial role in the development of stroke. However, little is currently known about the effects of adropin on the blood-brain barrier (BBB) function after intracerebral hemorrhage (ICH). In this study, the role of adropin in collagenase-induced ICH was investigated in mice.

Hematoma Expansion Following Intracerebral Hemorrhage: Mechanisms Targeting the Coagulation Cascade and Platelet Activation.

Hematoma expansion (HE), defined as a greater than 33% increase in intracerebral hemorrhage (ICH) volume within the first 24 hours, results in significant neurological deficits, and enhancement of ICH-induced primary and secondary brain injury. An escalation in the use of oral anticoagulants has led to a surge in the incidences of oral anticoagulation-associated ICH (OAT-ICH), which has been associated with a greater risk for HE and worse functional outcomes following ICH. The oral anticoagulants in use include vitamin K antagonists, and direct thrombin and factor Xa inhibitors.

Fucoidan from Fucus vesiculosus Fails to Improve Outcomes Following Intracerebral Hemorrhage in Mice.

Intracerebral hemorrhage (ICH) is the most fatal stroke subtype, with no effective therapies. Hematoma expansion and inflammation play major roles in the pathophysiology of ICH, contributing to primary and secondary brain injury, respectively. Fucoidan, a polysaccharide from the brown seaweed Fucus vesiculosus, has been reported to activate a platelet receptor that may function in limiting bleeding, and to exhibit anti-inflammatory effects.

Angiopoietin-like 4: A double-edged sword in atherosclerosis and ischemic stroke?

Ischemic stroke is one of the leading causes of death in the world, and thus is a major public health concern. Atherosclerosis, also known as atherogenesis, is a crucial risk factor for cerebral ischemia, yet how it develops remains largely unknown. It has been found, however, that angiopoietin-like protein 4 (ANGPTL4), a protein expressed in vascular endothelial cells, plays a role in the pathophysiology of atherosclerosis and may therefore be involved in ischemic stroke.