Research More Info 20

Title





Comment from Dr. Mladenoff


NFkappaB is the beginning of the inflammatory gene response that is expressed as cytokines, adhesion molecules, inflammtory enzyme, INOs, COX Enzymes and Lipoxigenase.


 The ability to modulate and down regulate activation of NFKappaB is essential in inflammation of any kind especially neuroinflammation results from head trauma.


This study concludes that taking the anti-oxidant N-acetylcysteine like CereNAC will inhibit NFKappaB translocation and Cox-2 expression. 


It is imperative to begin taking N-acetylcysteine like CereNAC as soon as possible after a concussion of any magnitude
Regulation of cyclooxygenase-2 expression in human osteoblastic cells by N-acetylcysteine. J Lab Clin Med. 2000 Nov;136(5):390-4.
Origuchi T1, Migita K, Nakashima T, Honda S, Yamasaki S, Hida A, Kawakami A, Aoyagi T, Kawabe Y, Eguchi K.

Abstract:  
Cyclooxygenase (COX) plays a pivotal role in the inflammatory process of inflammatory arthropathies. Inflammatory cytokines induce COX-2 expression in osteoblasts of inflamed joints, followed by osteoclast activation. The inhibition of COX-2 expression could help prevent prostaglandin E2 secretion, followed by osteoclast activation for bone destruction and resorption.

We examined whether the antioxidant N-acetylcysteine (NAC) inhibited COX-2 expression induced in the human osteoblastic cell line MG63 by interleukin-1beta (IL-1beta). According to Western blot and reverse transcription-polymerase chain reaction (RT-PCR) test results, NAC inhibited IL-1beta-induced COX-2 expression in protein and messenger RNA.

We also demonstrated immunohistochemically that NAC inhibited NFkappaB nuclear translocation. These results suggested that NAC inhibited both COX-2 expression and NFkappaB nuclear translocation in MG63, which in turn indicated that NAC could inhibit the inflammatory process involved in bone resorption by regulating COX-2 expression at the level of transcription.
Share by: