Emmez, GokcenBulduk, Erkut BahaYildirim, ZuhalSurgical Sciences2024-07-052024-07-05202211306-696X1307-794510.14744/tjtes.2021.019542-s2.0-85131262300https://doi.org/10.14744/tjtes.2021.01954https://hdl.handle.net/20.500.14411/1746bulduk, erkut baha/0000-0002-8812-1290BACKGROUND: Traumatic brain injuries cause damages in the brain in several ways, which include cell death because of edema, disruption of the blood-brain barrier, shear stress, and ischemia. In this study, we investigated the effects of adrenomedullin (AM) on oxidative stress and inflammation after head traumas in a rat model. METHODS: Eighteen male adult Wistar albino rats were randomized into three groups (n=6). No traumas were applied to the control (C) group. Traumas were applied in line with Marmarau trauma model in the trauma group. The rats in the AM treatment group were treated with post-traumatic 12 mu g/kg i.p. AM in addition to the trauma group. The rats were followed for 7 days in all groups and were then sacrificed. Brain tissues and blood samples were taken. RESULTS: In the trauma group, both tissue and serum MDA, TNF-alpha, and IL-6 levels were significantly increased compared to the control group (p<0.05). In the AM-treated group, serum TNF-alpha levels were significantly decreased compared to the trauma group (p<0.05). In the trauma group, both tissue and serum GSH levels were significantly decreased compared to the control group (p<0.05). In the trauma group, serum Vitamin D3 levels were significantly decreased compared to the control group (p<0.05). In the AM-treated group, both tissue and serum GSH levels were significantly increased compared to the trauma group (p<0.05). CONCLUSION: These results indicate that AM has neuroprotective effects on traumatic brain injury in a rat model.eninfo:eu-repo/semantics/openAccessAdrenomedullininflammationoxidative stresstraumatic brain injuryArticleQ4Q3286736742WOS:000809604900004356528611138197