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Present results demonstrate that OT appears to alleviate harmful effects of hyperglycemia on peripheral neurons by suppressing inflammation, oxidative stress and apoptotic pathways.

The aim of this study was to evaluate the effects of metoprolol, lipid emulsion and MgSO which can be recommended for prevention of long QT that is one of the lethal consequences of amitriptyline intoxication. Thirty Sprague-Dawley male rats were included. Five groups respectively received the following: saline intraperitoneally (i.p.); amitriptyline (AMT) 100 mg/kg per os (p.o.) and saline i.p.; AMT 100 mg/kg p.o. and 5 mg/kg metoprolol i.p.; AMT 100 mg/kg p.o. and 20 ml/kg lipid emulsion i.p.; AMT 100 mg/kg p.o. and 75 mg/kg MgSO i.p. After 1 h, all groups were analysed by ECG recordings in DII lead; their blood was taken for biochemical examination and euthanasia was performed. For histological examination, cardiac tissues were removed and sections were prepared. QTc was significantly reduced in treatment groups compared to the AMT+saline group. When compared with the AMT+saline, lipid emulsion did not affect pro-BNP and troponin levels in biochemical analysis, but it significantly reduced Caspase 3 expression in histological examination. In the group treated with AMT and metoprolol, there was no significant effect on Caspase 3 expression. In MgSO-treated group, there was a significant decrease in troponin, pro-BNP and urea levels biochemically and significant decrease in Caspase 3 expression histologically when compared with the control group. With further studies including clinical studies, MgSO, lipid emulsion or metoprolol may be used to improve AMT-induced cardiotoxicity. They can possibly become alternative approaches in the future for suicidal or accidental intoxication of tricyclic antidepressant in emergency departments.

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AIM: Sepsis is a systemic infection reaction and intravascular volume therapy plays a crucial role in it's treatment. Acute respiratory distress syndrome (ARDS) occurs in the lungs, the most affected organ. This study aimed to investigate the different effects of fl uid therapy on ARDS caused by sepsis. METHOD: To form a sepsis model, cecal ligation and puncture (CLP) procedure were performed on 44 adult rats. Divided into six groups; normal, CLP group, those treated with 40 ml/kg 0.9 % NaCl, 3 % NaCl (hypertonic saline), Ringer Lactate and Hydroxyethyl starch. After 24 hours treatments, histopathological examination of the lungs were done, and the plasma levels of CRP, TNF-α and IL-6 and paO 2 were measured. RESULTS: The scores of all histological parameters of the group treated with hypertonic saline were signifi cantly lower than of the other groups (p < 0.001). Likewise, according to the arterial blood gas results, paO 2 was signifi cantly higher (p < 0.01) in the hypertonic saline group compared to the other groups, and paCO 2 was signifi cantly lower (p < 0.01). CRP, TNF-α and IL-6 levels of infl ammatory markers were also signifi cantly lower in hypertonic saline groups compared to other groups (p < 0.001). CONCLUSIONS: Our study shows that treatment with hypertonic saline reduces the progression of ARDS in sepsis (Tab.

Purpose: Digitoxin is a cardiac glycoside used in the treatment of heart failure. Inspired by its known antiinflammatory effect, this study aims to investigate the effect of digoxin in a sepsis model and to bring to light its effect and underlying mechanism in acute lung injury (ALI). Method: 28 wistar albino rats were divided into 4 groups. Sepsis model is performed by the feces intraperitoneal-injection procedure (FIP). Results: TNF-a, CRP, IL-6, IL 1-Beta, lactic acid, and MDA values were significantly decreased in the FIP+digitoxin group compared to the FIP+Saline group. When the same groups were examined, histological improvements such as decrease in alveolar inflammation and decrease in septal thickening in the digitoxin group and thorax CT were found to be significantly higher in the Hounsfield unit digitoxin group compared to the Saline group. Conclusion: Digitoxin has shown biochemical improvement in sepsis with all known mechanisms of action, and healing effects in both computerized tomography and histology in the lung.

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Increased concentration of manganese (Mn) in the brain is known to be associated with excitotoxicity and neuroinflammation. Vinpocetine, an alkaloid derived from the plant Vinca minor L., basically shows its effect via phosphodiesterase inhibition and voltage-dependent Na channels. Vasoactive intestinal peptide (VIP) has gastrointestinal, vasomotor, muscular, and neuroprotective effects. The aim of this study was to examine the potential protective effects of vinpocetine and VIP against Mn toxicity in NE-4C neural stem cells (NSCs). VIP treatment at 1 μM and vinpocetine treatment at 2 μM concentrations were sufficient to yield maximum protection, and these concentrations were adopted in the following experiments. In this study, Mn treatment significantly increased lactate dehydrogenase (LDH) leakage, reactive oxygen species (ROS) production, and triggered cell death in NE-4C cultures. However, significant reduction in LDH release was observed following vinpocetine or VIP treatments when compared with control. Similar to these findings, vinpocetine or VIP treatments significantly reduced membrane degradation induced by Mn (p < 0.001). Moreover, vinpocetine attenuated Mn-induced decrease of mitochondrial membrane potential. Similarly, proapoptotic protein bax and ROS production significantly decreased in cells after incubation with vinpocetine (p = 0.01) or VIP in the presence of Mn (p < 0.001). Our study provides the evidence that both vinpocetine and VIP may exert protective effects via modulating oxidative stress and apoptosis in Mn-induced neurodegeneration in NE-4C cells.