Can thiamine pyrophosphate prevent desflurane induced hepatotoxicity in rats?

Cetin, Nihal/0000-0003-3233-8009; Arslan, Aynur/0000-0001-5968-5823; yilmaz, adnan/0000-0003-4842-1173WOS: 000374189100004PubMed: 27050787PURPOSE: To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS: Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG), TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. the oxidant/antioxidant levels and ALT, AST and LDH activities were measured. the histopathological examinations were performed in the liver tissues for all rats. RESULTS: Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). on contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSION: Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.Erzincan University Scientific Research Projects DepartmentErzincan Binali Yildirim University [SAG-B-080715-0173]Erzincan University Scientific Research Projects Department (Project no SAG-B-080715-0173

Can endocan be a new biomarker in ventilator-associated pneumonia?

Ventilator-Associated Pneumonia (VAP) is a hospital-acquired bacterial infection with high incidence and mortality rate. The aim of this study is to investigate the correlation between the Endocan level and development of VAP and whether or not this correlation was correlated with the clinical findings. Demographic data, white blood cell (WBC) count, procalcitonin (PCT), c-reactive protein (CRP), and fever levels of 60 patients were recorded in serial measurements for 5 days. When there was the presence of fever or elevated Endocan, alveolar lavage culture was taken and chest radiographies were taken. Correlations of the Endocan levels with the culture results and laboratory values were examined. The rate of VAP was found as 10.4/1000 mechanical ventilator days. Endocan levels were significantly higher in patients with VAP (p  0.05). No correlation was found between Endocan levels and PCT, WBC and CRP levels in those with VAP (p > 0.05). A significant correlation was found between the Endocan level and the elevated fever 24 h later (p:0.001). The serum Endocan level on the day 3 had a specificity of 73.3%, a sensitivity of 68.9%, positive predictive value of 44%, and negative predictive value of 88.5% at the cut off level of 9.17 ng/mL. In this study, it was determined that high Endocan levels were associated with the development of VAP. The present study suggested that Endocan can be used as a screening tool for the development of VAP. Clinical Trials.gov ID: NCT02916277. Keywords: Biomarker, Endocan, Ventilator-associated pneumoni

The Effect of Etoricoxib on Hepatic Ischemia-Reperfusion Injury in Rats

Ischemia-reperfusion (I/R) damage is known to be a pathological process which continues with the increase of oxidants and expands with the inflammatory response. There is not any study about protective effect of etoricoxib on the liver I/R damage in literature. Objective. This study investigates the effect of etoricoxib on oxidative stress induced by I/R of the rat liver. Material and Methods. Experimental animals were divided into four groups as liver I/R control (LIRC), 50 mg/kg etoricoxib + liver I/R (ETO-50), 100 mg/kg etoricoxib + liver I/R (ETO-100), and healthy group (HG). ETO-50 and ETO-100 groups were administered etoricoxib, while LIRC and HG groups were orally given distilled water by gavage. Hepatic artery was clamped for one hour to provide ischemia, and then reperfusion was provided for 6 hours. Oxidant, antioxidant, and COX-2 gene expressions were studied in the liver tissues. ALT and AST were measured. Results. Etoricoxib in 50 and 100 mg/kg doses changed the levels of oxidant/antioxidant parameters such as MDA, MPO, tGSH, GSHRd, GST, SOD, NO, and 8-OH/Gua in favour of antioxidants. Furthermore, etoricoxib prevented increase of COX-2 gene expression and ALT and AST levels. This important protective effect of etoricoxib on the rat liver I/R can be tested in the clinical setting

Liv-52; Prophylactic or therapeutic agent against desflurane-induced hepatotoxicity in rats

Cetin, Nihal/0000-0003-3233-8009WOS: 000383364400013Liv-52 has hepatoprotective effect and may be beneficial for desflurane hepatotoxicity. We aimed to investigate the prophylactic or therapeutic effects of Liv-52 on hepatotoxicity induced desflurane. the study was designed into seven groups as healthy group (HG), desflurane control groups (DCG-1, DCG-2, and DCG-3), Liv-52 treatment after desflurane (DLG), Liv-52 treatment before desflurane group (LDG), and Liv-52 treatment before and after desflurane group (LDLG). Desflurane was adjusted as to 6 % concentration for two hours. Liv-52 was given 20 mg/kg. Alanine transaminase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), malondialdehyde (MDA), and total glutathione (tGSH) levels were measured. MDA, tGSH, ALT, AST, and LDH levels of DLG, LDG, and LDLG were found statistically significant compared to controls and healthy groups (p 0.05). Pathological findings such as sinusoidal dilatation congestion and inflammation areas were observed in control groups but not in LDLG. Both prophylactic and therapeutic uses of Liv-52 may be the most appropriate methods to be minimized desflurane-induced hepatotoxicity.Erzincan University Scientific Research Projects Department [SAG-B-080715-0173]This research was supported by Erzincan University Scientific Research Projects Department. Project number is SAG-B-080715-0173

Effect of melatonin on antioxidant capacity, ınflammation and apoptotic cell death in lung tissue of diabetic rats

<div><p>Abstract Purpose: To investigate the effects of melatonin on antioxidant capacity, inflammation and apoptotic cell death (through expression of cleaved-caspase 3) in lung tissue samples of diabetic rats. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control group) was made up of healthy rats. Group 2 (diabetes group) received streptozotocin at a dose of 50 mg/kg/day for 5 days.Group 3 (diabetes plus melatonin group) received streptozotocin at a dose of 50 mg/kg/day for 5 days and then they received melatonin at a dose of 20 mg/kg/day between 28thand 35thdays of the study. Results: Tissue MDA and MPO levels were found to be significantly higher in diabetes group compared to control group (p<0.05) whilst administration of melatonin was found to significantly lower this increase down to normal levels (p<0.05). Bronchus associated lymphoid tissue (BALT) was more severe in diabetics whereas administration of melatonin alleviated this hyperplasia. Cleaved caspase 3 activity was severe in hyperplastic BALT in diabetic rats however in lowered down to moderate level when melatonin was administered. Conclusion: The melatonin caused an increase in antioxidant capacity and decreased the expression of cleaved-caspase 3.</p></div