Stroke is a neurological disorder characterized by blockage of blood vessels. Clots form in the brain and interrupt blood flow, clogging arteries and causing blood vessels to break, leading to bleeding. Rupture of the arteries leading to the brain during stroke results in the sudden death of brain cells owing to a lack of oxygen. Stroke can also lead to depression and dementia.
Ischemic stroke occurs because of a loss of blood supply to part of the brain, initiating the ischemic cascade. Brain tissue ceases to function if deprived of oxygen for more than 60 to 90 seconds, and after approximately three hours will suffer irreversible injury possibly leading to the death of the tissue, i.e., infarction.
As oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is the release of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane. However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result, the transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates enzymes that digest the cells' proteins, lipids, and nuclear material. Calcium influx can also lead to the failure of mitochondria, which can lead further toward energy depletion and may trigger cell death due to programmed cell death. In addition to damaging effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down collagen, hyaluronic acid, and other elements of connective tissue. The loss of vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which can cause secondary progression of the brain injury.
Matrix metallopeptidase 9 (MMP-9), also known as 92 kDa type IV collagenase, 92 kDa gelatinase or gelatinase B (GELB), is a matrixin, a class of enzymes that belong to the zinc-metalloproteinases family involved in the degradation of the extracellular matrix. Previous investigations demonstrated that an abnormal expression of MMP-2 (gelatinase A) or MMP-9 (gelatinase B) appears after cerebral ischemia and in lipopolysaccharide-injured brains, contributing to brain injury and BBB breakdown.
| Cat. No | Product Name | Reactivity | Application |
| CPBT-65227SH | Anti-MMP9 polyclonal antibody | H | WB, IHC-P |
| CABT-L2062 | Anti-Human MMP-9 Monoclonal Antibody, clone 27 | H | WB |
| CABT-L2467 | Anti-Mouse MMP-9 polyclonal antibody | M | ELISA, WB, IHC, IP |
S100 calcium-binding protein B (S100B) is a protein of the S-100 protein family. S100 proteins are localized in the cytoplasm and nucleus of a wide range of cells, and involved in the regulation of a number of cellular processes such as cell cycle progression and differentiation. S100B has emerged as a candidate peripheral biomarker of blood–brain barrier (BBB) permeability and CNS injury.
| Cat. No | Product Name | Reactivity | Application |
| DMABT-H27120H | Anti-S100B monoclonal antibody, clone TD68-13 | H, M, R, G, Z | WB, ICC/IF, IP, IHC |
| CABT-12099MH | Anti-S100B monoclonal antibody, clone 2C3 | H | WB, IHC, ELISA |
| DCABH-13354 | Anti-S100B monoclonal antibody, clone 2B20 | H | WB, ELISA |
Glial fibrillary acidic protein (GFAP) is considered to be a highly specific marker for glia. It is a type III intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS), including astrocytes and ependymal cells during development.
| Cat. No | Product Name | Reactivity | Application |
| DPABH-19078 | Anti-GFAP polyclonal antibody | H, R | WB, ELISA, IHC-P, ICC/IF |
| CPBT-66669GH | Anti-GFAP (C-terminal) polyclonal antibody | H, M, R, D | WB, ELISA |
| CABT-BL8484 | Anti-GFAP (C-terminal) monoclonal antibody, clone SN393 | H, M | IHC, WB |
The protein neuron-specific enolase (NSE), is expressed by mature neurons and cells of neuronal origin. Under normal physiological conditions, NSE is not secreted into extracellular space, however, during cellular injury or death, NSE can be both leaked into the extracellular space and up-regulated in response to the damaged neuronal tissue. NSE has been used as a biomarker in numerous pathological conditions in humans. NSE is also reported as a promising therapeutic target in acute spinal cord injury.
| Cat. No | Product Name | Reactivity | Application |
| DPAB1979RH | Anti-NSE polyclonal antibody | H | IHC |
| DMAB-L21045 | Anti-Human NSE monoclonal antibody, clone 712 | H | ELISA |
| CABT-BL8799 | Anti-Enolase (NSE) polyclonal antibody | H | ELISA, IP, WB |
| CABT-L724 | Anti-NSE monoclonal antibody, clone TD17-39 | H, M, R, Z | WB, ICC, IHC, FC |
Species: H Human; M Mouse; R Rat; Z Zebrafish; X Xenopus laevis; B Bovine; C Cow; D Dog; P Pig; Q Quail
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