Background: Brain injury often occurs not only primary brain injury, but often also occur secondary brain injury. Inflammation is a process that occurs immediately after trauma characterized by activation of the mediator substance. TNF-Î± is a major cytokinee involved in the inflammatory processes that have adverse effects if the serum level are excessive. There needs to be a balance of the inflammatory process in the brain injury so things that harm does not occur. As anti-inflammatory IL-10 plays an important role in maintaining the balance. The objective of this study is to determine the effect of IL-10 intervention as an anti-inflammatory will decrease the serum level of TNF-Î± in traumatic brain injury. Material And Method: Experimental Study in the Rattus Wistar Â rats, post test control group design, male, aged 3-4 months, with body weight (BW) 300-400g, were obtained from the Laboratory Animal Faculty of Medicine, University of Hasanuddin as much as 24 tails, which is the result of breeding. Subjects were divided into four groups, each group of six rats, treated with controlled cortical impact model (Feeneyâ€™s weight-drop) of traumatic brain injury. Blood taken with capillary tube in retro-orbita plexus or sinus.This study has approved by ethical clearance for research. Results: Levels of TNF-Î± group of rats 1 hour post-trauma without administration of recombinant IL-10 (28.58 Â± 7.28) pg / mL; was significantly higher (p <0.05) than the levels of TNF-Î± rats without kraniektomi group (22.06 Â± 3.34) pg / mL and group kraniektomi rats without brain injury (23.07 Â± 2.51) pg / mL. Levels of TNF-Î± group of rats 1 hour post-trauma by administration of recombinant IL-10 (23.39 Â± 6.30) pg / mL; significantly lower (p <0.05) than the group of rats 1 hour post-trauma without administration of recombinant IL-10; and did not different significantly (p> 0.05) in the group without craniectomy or craniectomy group without head injury. Conclusions: Â Intervention of recombinant IL-10 decreases levels of TNF-Î± serum soon after traumatic brain injury in rats.