Oxidative stress causes nuclear factor-κB activation in acute hypovolemic hemorrhagic shock

Efferent Vagal Fibre Stimulation Blunts Nuclear Factor-κB Activation and Protects Against Hypovolemic Hemorrhagic Shock

“…[3][4][5][6] Inactive NF-B is present in the cytoplasm complexed with the inhibitory protein IB␣. NF-B is activated by several incoming signals from the cell surface.…”

“…Nuclear and cytoplasmatic proteins were isolated as previously described. 6 Electrophoretic Mobility Shift Assay NF-B binding activity was performed as previously reported. 6 The binding bands were quantified by scanning densitometry of a bio-image analysis system (Bio-Profil Celbio).…”

“…6 The IB␣ protein signal was quantified by scanning densitometry using a bio-image analysis system (Bio-Profil). The results from each experimental group were expressed as relative integrated intensity compared with normal livers measured with the same batch.…”

“…4 -6 This inflammatory cascade causes a marked production of tumor necrosis factor-␣ (TNF-␣) that plays a pivotal role in the vascular failure and in the end-organ damage of acute hypovolemic shock. 5,6 The central nervous system modulates systemic inflammatory responses to various stressors through humoral mechanisms. [7][8][9] Stimulation of afferent vagus nerve fibers by cytokines or endotoxin stimulates pituitary-adrenal antiinflammatory responses 10 -12 ; however, a role of efferent vagus nerve signaling also exists in modulating inflammation.…”

Antioxidant Strategies in Neurocritical Care

“…Increased production of ROS and RNS during critical illness may be related to Ca ++ activation of phospholipase leading to intracellular accumulation of Ca ++ and excitotoxicity; activation of NOS and production of nitric oxide (NO); activation of phagocytes, release of iron, copper, and metalloproteins; conversion of xanthine dehydrogenase to xanthine oxidase; activation of eicosanoid pathway and inflammatory response; release of cytokines and expression of adhesion molecules nuclear factor-kappaB (NF-κB) and mitochondrial failure [2,[8][9][10]. High levels of ROS and intracellular Ca ++ overload can lead to structural alteration of the mitochondria and electron transport chain, resulting in further increase in ROS generation, and ROS reacts with fatty acids leading to lipid peroxidation and cell membrane damage.…”