Asset Details
Do you wish to reserve the book?
Selective Brain Cooling in Rats Ameliorates Intracerebral Hemorrhage and Edema Caused by Penetrating Brain Injury: Possible Involvement of Heme Oxygenase-1 Expression
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Selective Brain Cooling in Rats Ameliorates Intracerebral Hemorrhage and Edema Caused by Penetrating Brain Injury: Possible Involvement of Heme Oxygenase-1 Expression
Do you wish to request the book?
Selective Brain Cooling in Rats Ameliorates Intracerebral Hemorrhage and Edema Caused by Penetrating Brain Injury: Possible Involvement of Heme Oxygenase-1 Expression
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Selective Brain Cooling in Rats Ameliorates Intracerebral Hemorrhage and Edema Caused by Penetrating Brain Injury: Possible Involvement of Heme Oxygenase-1 Expression
2011
Overview
Brain edema formation associated with trauma-induced intracerebral hemorrhage (ICH) is a clinical complication with high mortality. Studies have shown that heme oxygenase-1 (HO-1) plays an important role in ICH-induced brain edema. In order to understand the role of HO-1 in the protective effect of selective brain cooling (SBC), we investigated the time course of HO-1 changes following penetrating ballistic-like brain injury (PBBI) in rats. Samples were collected from injured and control animals at 6, 24, 48, and 72 h, and 7 days post-injury to evaluate HO-1 expression, heme concentration, brain water content, and immunohistochemistry (IHC). Following a 10% frontal PBBI, HO-1 mRNA and protein was increased at all time points studied, reaching maximum expression levels at 24–48 h post-injury. An increase in the heme concentration and the development of brain edema coincided with the upregulation of HO-1 mRNA and protein during the 7-day post-injury period. SBC significantly decreased PBBI-induced heme concentration, attenuated HO-1 upregulation, and concomitantly reduced brain water content. These results suggest that the neuroprotective effects of SBC may be partially mediated by reducing the heme accumulation, which reduced injury-mediated upregulation of HO-1, and in turn ameliorated edema formation. Collectively, these results suggest a potential value of HO-1 as a diagnostic and/or therapeutic biomarker in hemorrhagic brain injury.
Publisher
SAGE Publications,Mary Ann Liebert, Inc
Subject
/ Brain
/ Brain Edema - physiopathology
/ Cerebral Hemorrhage - enzymology
/ Cerebral Hemorrhage - physiopathology
/ Cerebral Hemorrhage - therapy
/ Down-Regulation - physiology
/ Dropsy
/ Edema
/ Head Injuries, Penetrating - complications
/ Head Injuries, Penetrating - enzymology
/ Head Injuries, Penetrating - therapy
/ Heme
/ Heme - antagonists & inhibitors
/ Heme Oxygenase (Decyclizing) - biosynthesis
/ Heme Oxygenase (Decyclizing) - genetics
/ Heme Oxygenase (Decyclizing) - physiology
/ Hypothermia, Induced - methods
/ Injuries
/ Male
/ Neuroprotective Agents - pharmacology
/ Rats
/ Trauma
