Th hemolysate and hydrogen peroxide, the levels of lipid peroxide andTh hemolysate and hydrogen peroxide,

Th hemolysate and hydrogen peroxide, the levels of lipid peroxide and
Th hemolysate and hydrogen peroxide, the levels of lipid peroxide and amounts of arachidonic acid release were also analyzed. Three hours after the onset of Lasalocid (sodium) chemical information experimental SAH, 18 Japanese White rabbits received an injection of saline, trehalose, or maltose into the cisterna magna. Angiographic and histological analyses of the basilar arteries were performed. In a separate study, the femoral arteries from 60 rats were exposed to fresh autologous blood. At 1, 3, 5, 7, 10, and 20 days after treatment, cryosections prepared from the femoral arteries were histologically analyzed. Results: When cells were treated with hemolysate, trehalose inhibited the production of several inflammatory mediators and degradation of the inhibitor of NF-B and also suppressed the lipid peroxidation, the reactive oxygen species-induced arachidonic acid release in vitro. In the rabbit model, trehalose PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27488460 produced an inhibitory effect on vasospasm after the onset of experimental SAH, while maltose had only a moderate effect. When the rat femoral arteries exposed to blood were investigated for 20 days, histological analysis revealed that trehalose suppressed vasospasm, inflammatory response, and lipid peroxidation. Conclusions: These data suggest that trehalose has suppressive effects on several pathological events after SAH, including vasospasm, inflammatory responses, and lipid peroxidation. Trehalose may be a new therapeutic approach for treatment of complications after SAH. Keywords: Trehalose, Subarachnoid hemorrhage, Cerebral vasospasm, Inflammatory response, Oxidative stress* Correspondence: [email protected] Equal contributors 2 NEXT21 K.K., 3-38-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan 3 Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan Full list of author information is available at the end of the article?2012 Echigo et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Echigo et al. Journal of Translational Medicine 2012, 10:80 http://www.translational-medicine.com/content/10/1/Page 2 ofBackground Aneurysmal subarachnoid hemorrhage (SAH) is a serious condition which often leads to high mortality and morbidity [1]. Ischemic injury due to cerebral vasospasm is a major cause of brain damage after SAH. However, cerebral vasospasm is only considered one of the underlying causes of SAH, and does not represent all of the associated clinical manifestations. A recent study also demonstrated that recovery of vasoconstriction by an endothelin antagonist did not necessarily contribute to improved clinical outcome [2], and additional mechanisms of secondary injury besides vasospasm have been suggested [3]. SAH occurs after the rupture of an aneurysm on the cerebral artery wall. Erythrocyte cytosol is released into the subarachnoid space through hemolysis of erythrocytes. Oxyhemoglobin or a related high molecular weight compound in erythrocyte cytosol can elicit a wide range of stress responses, including activation of inflammatory responses and production of inflammatory cytokines [4]. These actions are partially regulated by the NF-B signaling pathway. The NF-B signaling pathway is essential for host defense and.