Empirical Study On The Expression Of Nuclear Factor-kappa B And ICAM-1 In Rats After Brain Injury And The Treatment With Insulin

Objective: Traumatic brain injury is a common disease , it is an endanger to mankind, and the case fatality rate is very high. It is a challenge for medical members to prevent and cure the secondary brain injury efficiently. The investigation indicated that nuclear factor-kappa B regulate the dilivery of lots of mediators of inflammation, and it played an important role in secondary brain injury.In addition, Intercellular adhesion molecule-1 participate inflammatory reaction, the activation of intercellular adhesion molecule-1 can induce the up-regulation activity of nuclear factor-kappa B, nuclear factor-kappa B can also stimulate the expression of Intercellular adhesion molecule-1 and bring about reaction of cascade connection, and aggravate brain injury. In recent years, we find that central nervous system of vertebrate exist insulin, the receptors of insulin distribute in central nervous system, peripheral insulin can enter central nerve system through blood brain barrier. Besides, we find that insulin can protect postischemia neuron, its protection depends not only on lower blood glucose, but also on other pathway of protection. A research report that insulin inhibit the expression of ICAM-1 in arteriae aorta endotheliocyte, but it did not interpret its mechanism. The experiment is to explore the brain protection pathway of insulin by inhibiting NF - κB, and to investigate the effect of inflammation molecule and its...