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Stroke, the sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is lost by blockage or rupture of an artery to the brain, is also a leading cause of dementia and depression.

Stroke subtypes. Fig.1 Stroke subtypes. (Marsh, 2010)

Risk Factors for Stroke

Risk factors associated with stroke can be classified as either non-modifiable or potentially modifiable.

  • Hypertension
  • Poor dietary and physical activity habits
  • Tobacco
  • Alcohol
  • Diabetes, obesity, and dyslipidaemia
  • Cardiac causes
  • Psychosocial stress
  • Socioeconomic status
  • Air pollution and rapid weather changes

Cell Death in Stroke

Brain tissue can be severely damaged when the blood flow supply is reduced to less than 20%. The hypoxia leads to ATP depletion within minutes, inducing the failure of the Na+/K+ pump, neuronal depolarization, and release of glutamate. Because glutamate cannot be taken up by either neurons or astrocytes, levels of glutamate rapidly rise in the extracellular space, leading to activation of glutamate receptors (mainly N-Methyl-D-Aspartat Receptors, NMDAR) that allow the entrance of Ca2+. Increased intracellular Ca2+ activates calpains and phospholipases, leading to excitotoxic cell death.

Major pathways implicated in ischaemic cell death: excitotoxicity, ionic imbalance, oxidative and nitrosative stresses, and apoptotic-like mechanisms. Fig.2 Major pathways implicated in ischaemic cell death: excitotoxicity, ionic imbalance, oxidative and nitrosative stresses, and apoptotic-like mechanisms. (Lo, 2003)

Selective Treatments for Multiple Stroke

  • Combination therapy
  • Most ischaemic strokes are caused by thromboembolic occlusions of major arteries that supply the brain. Agents that lyse these clots reperfuse the ischaemic brain and form the basis of thrombolytic therapy. Indeed, thrombolysis using recombinant tPA is currently the only therapy for acute stroke approved by the US Food and Drug Administration.

    In animal models, various neuroprotective combinations have been used with some success, including co-administration of an NMDA receptor antagonist with GABA (γ-aminobutyric acid) receptor agonists, free radical scavengers, citicholine, the protein synthesis inhibitor cycloheximide, caspase inhibitors, or growth factors such as basic fibroblast growth factor (bFGF).

  • Lessons from preconditioning
  • Two temporally distinct types of tolerance are induced by preconditioning stimuli: acute - observed within minutes and delayed - developing after hours. Preconditioning might offer insights into the molecular mechanisms responsible for endogenous neuroprotection, and so provide new strategies for making brain cells more resistant to ischaemic injury.

  • The microcirculation
  • Armed with the new knowledge that patients and experimental animals show improved outcomes after the early restoration of blood flow, many strategies have emerged that preserve cerebral blood flow and render the microcirculation more resistant to acute ischaemic injury. Among the most promising methods to enhance nitric oxide synthesis by the vascular endothelium, both increasing vascular endothelial NOS expression or increasing NOS enzymatic activity seems to be effective in experimental models.

Therapeutic targets for microcirculation. Fig.3 Therapeutic targets for microcirculation. (Lo, 2003)

Products We Can Provide for Stroke Research

Target name Product name Cat. No.
NMDA Amantadine hydrochloride [NMDA Antagonist] MOD2005ZP370
NMDA DL-AP5 sodium salt [NMDA Antagonist] MOD2005ZP373
GABA Guinea pig Anti-GABA Polyclonal Antibody, Unconjugated NAB-0720-Z1907
CREB CREB1 pS133 / CREB1 ELISA Kit [Colorimetric] NPP2011ZP375
CREB CREBtide Peptide NPP2012442CR
CREB Mouse CREB Antibody NAB-2102-MP965
TXA2 Human Recombinant TP Prostanoid Receptor Stable Cell Line NCL20120120CR
MMP Mouse Anti-Human MMP-3 Monoclonal Antibody (Clone F36P1B4), Unconjugated NAB2012281LS
MMP Mouse Anti-Human MMP-9 Monoclonal Antibody (Clone M2101G05), Unconjugated NAB2012426LS
MMP Mouse Anti-Human MMP-1 Monoclonal Antibody (Clone M4110F03 ), Unconjugated NAB2012433LS
ET-1 Rabbit Anti-ET-1 Polyclonal Antibody, Lot BS21-6P566 NAB-BA-P3882
ET-1 Mouse Anti-ET-1(2C4) Monoclonal Antibody (2C4) NAB-BA-P4046

Creative Biolabs is an innovative and experienced provider of neuroscience products and solutions. We use our state-of-the-art R&D expertise to help our clients develop outstanding research results in stroke. We want to contribute to better health in the world. Please contact us for more details.


  1. Marsh, J.D.; Keyrouz, S.G. Stroke prevention, and treatment. Journal of the American College of Cardiology. 2010, 56(9): 683-691.
  2. Lo, E.H.; et al. Mechanisms, challenges and opportunities in stroke. Nature reviews neuroscience. 2003, 4(5): 399-414.
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