title: Progesterone treatment inhibits the inflammatory agents that accompany traumatic brain injury.
abstract: Progesterone given after traumatic brain injury (TBI) has been shown to reduce the initial cytotoxic surge of inflammatory factors. We used Western blot techniques to analyze how progesterone might affect three inflammation-related factors common to TBI: complement factor C3 (C3), glial fibrillary acidic protein (GFAP), and nuclear factor kappa beta (NFkappaB). One hour after bilateral injury to the medial frontal cortex, adult male rats were given injections of progesterone (16 mg/kg) for 2 days. Brains were harvested 48 h post-TBI, proteins were extracted from samples, each of which contained tissue from both the contused and peri-contused areas, then measured by Western blot densitometry. Complete C3, GFAP, and NFkappaB p65 were increased in all injured animals. However, in animals given progesterone post-TBI, NFkappaB p65 and the inflammatory metabolites of C3 (9 kDa and 75 kDa) were decreased in comparison to vehicle-treated animals. Measures of NFkappaB p50 showed no change after injury or progesterone treatment, and progesterone did not alter the expression of GFAP. The therapeutic benefit of post-TBI progesterone administration may be due to its salutary effect on inflammatory proteins known to increase immune cell invasion and cerebral edema.
authors.affiliation: Department of Cell Biology, Emory University, Atlanta, GA 30322, USA.
authors.forename: Edward H
authors.initials: EH
authors.lastname: Pettus
authors.forename: David W
authors.initials: DW
authors.lastname: Wright
authors.forename: Donald G
authors.initials: DG
authors.lastname: Stein
authors.forename: Stuart W
authors.initials: SW
authors.lastname: Hoffman
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001930:Brain Injuries / Q000276:immunology / Q000378:metabolism*; D003176:Complement C3 / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology / Q000378:metabolism*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D008297:Male; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000627:therapeutic use; D011374:Progesterone / Q000276:immunology / Q000502:physiology* / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000893:Anti-Inflammatory Agents; D003176:Complement C3; D005904:Glial Fibrillary Acidic Protein; D016328:NF-kappa B; D018696:Neuroprotective Agents; D011374:Progesterone