Signal Transduction Mechanisms Underlying Regulation Of CCK-8 For Expression Of INOS Induced By LPS In ECV-304

Endotoxin shock is a common and severe pathological process with high mortality, and has been one of the most important topics in biomedicine. In clinical practice bacterial infections are the most common cause for endotoxin shock. However, in forensic practice endotoxin shock can be caused by severe trauma and vigorous stress stimulation, which can lead to decrease in systemic blood pressure and redistribution of blood volume, subsequential intestinal membrane ischemia and local immunologic dysfuntions resulting in the disorders of intestinal membrane barriers and intestinal-originated endotoxin lipopolysaccharide (LPS) translocation into blood.The disorders of vascular regulations is characteristic of endotoxin shock with the manifestations of marked reduction in systemic mean arterial pressure whereas pulmonary arterial hypertension, as well as abnormal changes of vascular reactivities of systemic and pulmonary arteries at its initial stage. It has been well known that vascular endothelial cells (VEC) are not only a mechanical and biological barrier of blood vessels, but also an endocrine organ, which maintain vascular normal tension and reactivities througth synthesis and release vasoactive substances such as nitric oxide (NO). NO, a first gas information molecule discovered in human being, is a typical endothelial-derived relaxant and mediates endothelium-dependent relaxation of blood vessels. In the pathogesis of endotoxin shock VEC is one of the major target cells of LPS and LPS-induced proinflammatory cytokine such as tumor necrosis factor and interlukin 1 and activated. In VEC inducible nitric oxide synthase (iNOS) is induced and lead to an increase in production of NO, the while endothelial nitric oxide synthase (eNOS) is inhibited and elicit decrease in NO formation, both of which are demonstrated to induce the...