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Article Citation - WoS: 4Citation - Scopus: 4Neuroprotective effects of adrenomedullin in experimental traumatic brain injury model in rats(Turkish Assoc Trauma Emergency Surgery, 2022) Emmez, Gokcen; Bulduk, Erkut Baha; Yildirim, ZuhalBACKGROUND: 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.Article Citation - WoS: 1Citation - Scopus: 2Cannabinoid Receptor Ligands Modulate Fibrosis and Inflammation in Idiopathic Pulmonary Fibrosis: a Preliminary Study(Tubitak Scientific & Technological Research Council Turkey, 2024) Kose, Sevil; Onen, Selin; Gizer, Merve; Boduroglu, Esin; Gonullu, Ugur; Korkusuz, PetekBackground/aim: No specific pharmacological treatment regimen for idiopathic pulmonary fibrosis (IPF) exists. Therefore, new antiinflammatory therapeutic strategies are needed. Cannabinoids (CBs), known for their inflammation-modulating and antifibrotic effects, may be potential medication candidates for treating IPF. We aim to evaluate the inflammation-modulating and antifibrotic effects of CB receptor (CBR) agonists and antagonists in lipopolysaccharide-stimulated normal human lung fibroblast, epithelial cells, IPF fibroblast cells, and monocytes. Materials and methods: We detected CBRs in normal human lung fibroblasts (LL24) and IPF fibroblast cells (LL29), epithelial cells (A549) and monocytes (THP-1) by flow cytometry. We determined TGF-(31, IL-8, and TNF-alpha inflammatory cytokines in the LL24, LL29, A549, and THP-1 cell culture supernatants on days 1 and 5 by ELISA. We evaluated the cell viability in LL24, LL29, and A549 cells on days 1, 3, and 5 spectrophotometrically and detected collagen Type I (ColI) production in the LL24 and LL29 cell culture supernatants on days 1, 3, and 5 by ELISA. Results: LL24, LL29, A549, and THP-1 cells exhibited CB1 (CB1R) and CB2 (CB2R) receptors. CB1R and CB2R agonists WIN55,2122 and JWH015 inhibited fibroblastic and epithelial cell proliferation on day 5. TGF-(31 and TNF-alpha release increased, while IL-8 release decreased in LL24, LL29, A549, and THP-1 cells in response to the administration of WIN55,212-2 and JWH015 at a 10-2 mM concentration. CB1R and CB2R antagonists AM251 and AM630 did not block agonistic responses, suggesting a nonclassical CBRmediated pathway. CB2R agonist JWH015 decreased ColI expression in IPF lung fibroblasts LL29 on day 3. Conclusion: These results suggest that CB signaling regulates the progression of pulmonary inflammation and fibrosis via CBR activation. This may offer a potential pharmacological tool for developing antifibrosis therapies.Article Citation - WoS: 3Citation - Scopus: 5Subclinical Inflammation Is Associated With Reductions in Muscle Oxygenation, Exercise Capacity and Quality of Life in Adults With Type 2 Diabetes(Elsevier, 2020) Bozdemir-Ozel, Cemile; Arikan, Hulya; Calik-Kutukcu, Ebru; Karaduz, Beyza Nur; Inal-Ince, Deniz; Kabakci, Giray; Dagdelen, SelcukObjectives: Exercise capacity is related to both morbidity and mortality in patients with type 2 diabetes (T2DM). The aim of this study was to investigate the relationship between subclinical inflammation level, exercise capacity, muscle oxygenation and quality of life in T2DM. Methods: This study includes 28 patients with T2DM (mean age, 51.5 +/- 5.0 years; male-to-female ratio, 6:22). Exercise capacity was evaluated using an incremental symptom-limited maximal exercise test on a bicycle ergometer. Muscle oxygenation was investigated using a wearable lactate-measuring device. Diabetes-specific quality of life was assessed using the Diabetes Quality of Life Questionnaire (DQOL). Subclinical inflammation was assessed using C-reactive protein (CRP) levels. Results: CRPlevelwasnegatively correlatedwith peakworkload during the test (r=-0.588, p=0.002), muscle oxygenation (r=-0.465, p= 0.019) and the psychological impact of treatment subscale of the DQOL (r= e0.540, p=0.017), and positively correlated with body mass index (r=0.519, p=0.008), waist circumference (r=0.426, p=0.038) and fat percentage (r=0.573, p=0.004). Therewasnocorrelation betweenCRPand fasting blood glucose or glycated hemoglobin level (p>0.05). Peakworkloadwas inversely related to fat percentage (r=-0.467, p=0.016) and the DQOLworry about the future impact of diabetes subscale (r=-0.501, p=0.021). Conclusions: In our study, subclinical inflammation negatively affected muscle oxygenation, exercise capacity and quality of life independently of glycemic indicators. Our findings suggest that the degree of glycemic control is insufficient to explain lower exercise capacity. Further studies are needed to investigate subclinical inflammation-reducing interventions in T2DM. (C) 2020 Canadian Diabetes Association.
