Inhibitory effect of progesterone on inflammatory factors after experimental traumatic brain injury.
OBJECTIVE
Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality in young people. Inflammatory cytokines play an important part in the pathophysiology of TBI. Recent studies demonstrate that progesterone significantly reduces cerebral edema and enhances functional recovery from TBI and stroke in several animal models. This study was designed to investigate the inhibitory effect of progesterone on inflammatory response after traumatic brain injury.


METHODS
Progesterone was injected intraperitoneally using rats as a model of traumatic brain injury, and Western blot technique was applied to detect the expression of three inflammation-related factors: nuclear factor kappa B p65 (NFkappaB p65), glial fibrillary acidic protein (GFAP), and tumor necrosis factor-alpha (TNF-alpha). The water content of injured brain was also examined. A neurological severity score was recorded to evaluate the effect of progesterone on neurodeficit recovery.


RESULTS
NFkappaB p65, GFAP, and TNF-alpha were increased in all injured animals. In rats treated with progesterone, the expression level of NFkappaB p65 and TNF-alpha were reduced significantly in comparison with vehicle-treated rats. However, progesterone did not alter the expression of GFAP in the injured rats. Progesterone also reduced the water content of injured brain and the lesion volume. In addition, progesterone-treated injured rats showed significant improvements in the Neurological Severity Score test, compared with vehicle-treated ones.


CONCLUSIONS
Progesterone inhibits the inflammatory response after experimental traumatic brain injury and mitigates the severity of brain damage.
Pan
De-Sheng
DS
Department of Neurosurgery, The First Affiliated Hospital, Medical College of Zhejiang University, Hangzhou 310003, Zhejiang, China.
Liu
Wei-Guo
WG
Yang
Xiao-Feng
XF
Cao
Fei
F
D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D001929:Brain Edema / Q000517:prevention & control; D001930:Brain Injuries / Q000188:drug therapy* / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000187:drug effects; D008297:Male; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D011374:Progesterone / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
D000199:Actins; D016328:NF-kappa B; D018696:Neuroprotective Agents; D014409:Tumor Necrosis Factor-alpha; D011374:Progesterone