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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: 2Citation - Scopus: 2Paraoxonase and Oxidative Stress Changes in Left and Right Ventricles of Exhaustively Exercised Rats(Canadian Science Publishing, 2021) Sarikaya, Badegul; Runa, Metin; Dayanir, Duygu; Gunduztepe, Yasemin; Pinar, LamiaExhaustive exercise can cause subclinical inflammation to the heart, as it is an oxidative tissue that works continuously. The effect of exhaustive exercise on left and right ventricles (LVs, RVs) may be different. It is claimed that paraoxonase-1 (PON1), an antioxidant enzyme, has a cardioprotective effect on oxidative stress. Rats were separated as non-exercised controls (Con), those euthanized immediately after (E-0) and 24 h after exhaustive exercise (E-24). Cardiac troponin-I (cTnI), total antioxidant status (TAS), total oxidant status (TOS), PON1 activities, and histological findings in LV and RV of the exhausted rats were evaluated. TAS and PON1 levels were lower in LVs compared with RVs of all groups. TOS levels were high in LVs compared with RVs of all groups. In LVs, TAS levels decreased significantly in the E-0 group while PON1 activity decreased in E-0 and E-24 groups compared with controls. In LVs, TOS levels decreased significantly in E-0 and E-24 groups, but in RVs a decrease was seen only in the E-0 group. cTnI levels increased significantly in the E-0 group and decreased to control levels in the E-24 group. Considering the histological and biochemical findings, exhaustive exercise affected the heart to the maximum during and just after exhaustion, and LV was influenced more than RV.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.
