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Abstract
Stroke is the second most fatal disease following cancer. Stroke occurs as a result of interruption of blood supply to a part of brain typically by a thrombus, embolus or hemorrhage that in turn lead to ischemia or reperfusion injury. Many risk factors have been identified as the probable cause for ischemia as cardiac diseases, smoking and genetic factors.
Apoptosis has been implicated in a wide range of pathological conditions. Ischemic injuries have been suggested to be accompanied by increased apoptosis, which lead to neuronal degeneration.
Apoptosis is the result of an active cellular response that can be elicited by a variety of stimuli like growth factor deprivation or molecular damage.
The apoptotic process can occur by either the internal or external pathway. The internal pathway is initiated by a variety of cytotoxic stimuli and mediated by the release of cytochrome c and subsequent activation of downstream caspases. The external pathway is mainly triggered by ligation of death receptors as Fas, TNF-related apoptosis including ligand-Ri (TRAIL-Ri), TRAIL-R2 and TNFR p55, and mediated by direct activation of upstream caspases.
The molecular components of apoptosis include positive (proapoptoti c) and negative (antiapoptotic) regulators.
Important molecules for the initiation of the apoptotic program in a variety of disease models are the death receptor Fas (CD95/Apo-1). A truncated form of the Fas receptor, the soluble Fas (sFas) may indicate activation of the Fas/Fas L system and act as a negative feedback mechanism thereby inhibiting Fas mediated apoptosis and reflecting the systemic tissue damage.
Tumor necrosis factor alpha (TNF-ct) is a pleiotropic cytokine that is produced by a variety of cell types. In addition to its role in host defense.