Cox‐2 Regulation Differs Between Sexes in the Secondary Inflammatory Response Following Experimental Penetrating Focal Brain Injury in Rats
Traumatic brain injury (TBI) is followed by secondary neuronal degeneration, largely dependent on an inflammatory response. This response is probably gender specific, since females are generally better protected than males in animal models and human epidemiological studies of TBI. The reasons are not fully known. We examined aspects of the inflammatory response following experimental TBI in male and female rats to explore possible gender differences. A penetrating brain injury model was used to produce focal TBI in male (n=10) and female (n=10) rats. After 24 h and 72 h the brains were removed and subjected to immunohistochemical analyses and in situ hybridization. Cox‐2 mRNA was elevated in the perilesional area compared to the un‐injured contralateral side, and significantly higher in males compared to females at 24 h and 72 h (p<0.05). iNOS mRNA and protein expression, GFAP, osteopontin, 3‐nitrotyrosine and Fluoro Jade positive cells were upregulated in the perilesional area at 24 h with no difference between sexes. Our findings showed a gender difference in posttraumatic Cox‐2 levels in Sprague‐Dawly rats. It is possible that the sex specific trait of the secondary inflammatory response may be connected to prostaglandin regulation rather than oxidative stress also in clinical contexts. The difference did, however, not correlate with altered neuronal death at 24 h. Astrogliosis and microgliosis did not differ between sexes. This heterogeneity comprises a sex dependent quality. The identification of gender specific post‐traumatic processes demonstrates a gender‐specific metabolic quality, which may partially explain variances in outcome after TBI.