Effect of mirtazapine on gastric oxidative stress and DNA injury created with methotrexate in rats

In this study, effect of mirtazapine on gastric oxidative stress and DNA injury created with methotrexate was investigated. Experimental results showed that GSH (nmol/g protein), MDA (?mol/g protein) and MPO (?/g protein) in the gastric tissue of the control group rats receiving methotrexate are 4.97 ± 0.37, 2.78 ± 0.30 and 3.12 ± 0.18, respectively. GSH, MDA and MPO measurements in the gastric tissue of rats receiving mirtazapine + methotrexate were detected to be 9.23 ± 0.51(p < 0.0001), 1.80 ± 0.31(p < 0.0001) and 1.63 ± 0.25 (p < 0.0001), respectively. GSH, MDA and MPO values in the intact rat group were found 8 ± 0.38 (p < 0,0001), 1.63 ± 0.28 (p < 0.0001) and 1.37 ± 0.21 (p < 0.0001), respectively. In addition, while 8-ohdG/dG quantity that DNA injury product in the control group administered methotrexate was 2.4 ± 0.11 pmol/L, this quantity was 1.3 ± 0.14 pmol/L (p < 0.001), 1.1 ± 0.10 pmol/L (p < 0.001) in mirtazapine and intact group, respectively. As a result, it was seen that mirtazapine prevents increase of oxidative stress and DNA injury created with methotreaxete in the gastric tissue of rat

High mobility group box protein-1 (HMGB-1) as a new diagnostic marker in patients with acute appendicitis

<p/> <p>Background</p> <p>The aim of this prospective study was therefore to evaluate the diagnostic value of preoperative serum High Mobility Group Box Protein-1 (HMGB-1) levels in patients with Acute Appendicitis (AA) who show normal white blood cell count (WBC) counts.</p> <p>Method</p> <p>Our study was carried out from October 2010 through November 2010 and included 20 healthy control group participants and 60 patients who presented at the emergency department of Erzurum Training and Research Hospital in Turkey with acute abdominal pain complaints, who were pathologically diagnosed with AA after laparotomy, and who agreed to participate in the study.</p> <p>Results</p> <p>Of the 60 patients who underwent appendectomies, 36 were male and 24 were female, and of the healthy group, 12 were male and 8 female. The age averages of the patients in Groups 1, 2 and 3 were, respectively, 31.3+15.4, 34.0+16.3 and 31.0+13.1 years. The WBC averages of Groups 1, 2 and 3 were, respectively, 7.41+2.02 (x10⁹/L), 15.71+2.85 (x10⁹/L) and 8.51+1.84 (x10⁹/L). The HMGB-1 levels for Groups 1 (healthy persons), 2 (AA patients with high WBC counts ) and 3 (AA patients with normal WBC counts) were, respectively, 21.71 ± 11.36, 37.28+13.37 and 36.5 ± 17.73 ng/ml. The average HMGB-1 level of the patients with AA was 36.92 ± 15.43 ng/ml while the average HMGB-1 value of the healthy group was 21.71 ± 11.36 ng/ml.</p> <p>Conclusion</p> <p>The significantly higher levels of HMGB-1 in AA patients compared to healthy persons infer that HMGB-1 might be useful in the diagnosis of AA. Use of HMGB-1, especially in patients with normal WBC counts, will reduce the number of unnecessary explorations.</p

A comparative investigation of biochemical and histopathological effects of thiamine and thiamine pyrophosphate on ischemia-reperfusion induced oxidative damage in rat ovarian tissue

Cetin, Nihal/0000-0003-3233-8009; Suleyman, Halis/0000-0002-9239-4099WOS: 000324122900012PubMed: 23760618In this study, the biochemical and histopathological effects of thiamine and thiamine pyrophosphate on ischemia-reperfusion induced oxidative damage in rat ovarian tissue were investigated. Animals were divided into four groups of six rat each, ovarian ischemia-reperfusion (IR), 25 mg/kg thiamine + ovarian ischemia-reperfusion (TIR), 25 mg/kg thiamine pyrophosphate + ovarian ischemia-reperfusion (TPIR) and Sham group (SG). the results of the biochemical experiments have shown that the rat ovarian tissue with thiamine treatment, the level of MDA, GSH and the 8-hydroxyguanine are almost the same as the IR group; while in the group with thiamine pyrophosphate treatment, the level of MDA, GSH and the 8-hydroxyguanine are almost the same as the SG. Ovarian tissue of rats in the IR group were congested and dilated vessels, edema, hemorrhage, necrotic and apoptotic cells. in this group, the migration and the adhesion of the polymorphonuclear leucocytes to the endothelium were observed. Both ovaries in TPIR group, there was no difference according to the SG. Histopathology of ovarian tissues in the TIR group was almost the same with the IR group. Our results indicate that thiamine pyrophosphate significantly prevents the ischemia-reperfusion induced oxidative damage in ovarian tissue, whereas thiamine has no effect. in conclusion, we have found that thiamine pyrophosphate prevents oxidative damage due to ischemia-reperfusion injury, whereas thiamine does not have this effect. Furthermore, we have confirmed that the results of our biochemical analyses are in concordance with the histopathological findings

Protective effect of nimesulide against hepatic ischemia/reperfusion injury in rats: Effects on oxidant/antioxidants, DNA mutation and COX-1/COX-2 levels

Yilmaz, Ismayil/0000-0001-7894-3613WOS: 000338395600018PubMed: 24948067Background: Nimesulide is a pharmacological agent and selective COX-2 inhibitor. It has anti-inflammatory, analgesic and antipyretic properties. the purpose of this study was to investigate the effect of nimesulide on oxidant/antioxidant, DNA mutation and COX-1/COX-2 activities in rat liver tissue with induced ischemia/reperfusion (I/R). Methods: Before the experiment, rats were divided into four groups; liver ischemia/reperfusion (LIR), 50 mg/kg nimesulide + liver ischemia/reperfusion (NLIR50), 100 mg/kg nimesulide + liver ischemia/reperfusion (NLIR100) and a control group to be given a sham operation (SG). Malondialdehyde (MDA), total glutathione (GSH) levels and myeloperoxidase (MPO), COX-1/COX-2 enzyme activities and DNA damage product level results from liver tissues and serum AST and ALT levels were determined. the data obtained were compared with the results from the liver ischemia/reperfusion and sham operation groups. Results: MDA levels, MPO and COX-2 activities and products of DNA injury were significantly lower in the groups given nimesulide, and particularly the NLIR100 group, compared to the LIR group (p 0.05). AST and ALT levels were significantly lower in the other groups compared to the LIR group (p < 0.05). Conclusions: Nimesulide at 100 mg/kg prevented oxidative liver damage induced with I/R significantly better than at a dose of 50 mg/kg. These experimental findings indicate that nimesulide may be useful in the treatment of hepatic I/R damage. (C) 2014 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Urban & Partner Sp. z o.o. All rights reserved

Effect of Mirtazapine on Gastric Oxidative Stress and DNA Injury Created With Methotrexate in Rats

In this study, effect of mirtazapine on gastric oxidative stress and DNA injury created with methotrexate was investigated. Experimental results showed that GSH (nmol/g protein), MDA (?mol/g protein) and MPO (?/g protein) in the gastric tissue of the control group rats receiving methotrexate are 4.97 ± 0.37, 2.78 ± 0.30 and 3.12 ± 0.18, respectively. GSH, MDA and MPO measurements in the gastric tissue of rats receiving mirtazapine + methotrexate were detected to be 9.23 ± 0.51(p < 0.0001), 1.80 ± 0.31(p < 0.0001) and 1.63 ± 0.25 (p < 0.0001), respectively. GSH, MDA and MPO values in the intact rat group were found 8 ± 0.38 (p < 0,0001), 1.63 ± 0.28 (p < 0.0001) and 1.37 ± 0.21 (p < 0.0001), respectively. In addition, while 8-ohdG/dG quantity that DNA injury product in the control group administered methotrexate was 2.4 ± 0.11 pmol/L, this quantity was 1.3 ± 0.14 pmol/L (p < 0.001), 1.1 ± 0.10 pmol/L (p < 0.001) in mirtazapine and intact group, respectively. As a result, it was seen that mirtazapine prevents increase of oxidative stress and DNA injury created with methotreaxete in the gastric tissue of rat

The Effect of Ozone Treatment on Thermal Burn Wound Healing; an Experimental Study

Objective: Ozone has been advised as a metabolic excitative in cell, immunomodulatory agent and antioxidant enzyme actuator. The present study was performedto designate the profit of ozone therapy on the burn wound healing in the rats.Methods: 40 adult Wistar type rats divided into 4 groups: a control group (burn notcreated and topical and systemic agents not used), a burn group (burn created but onlysaline given), a burn+silver sulfadiazine group (silver sulfadiazine was applied for 21days), a burn+ozone/oxygen mixture group (ozone/oxygen mixture was applied for 21days).After anesthetizing, second-degree burn (2 cm2areas) was done on the dorsal ofthe animals byaluminum plate in boiling hot water (100 ?C for 15 seconds) and othergroups except control group were treated topically, based on the time scheduled.Tissue samples were harvested on day 7st and 21st after burn injury. Biochemical andhistological analyzes were performed in tissue and blood samples. The results wereassessed with appropriate statistical tests and given as Means±SD.Results: The histopathologic damage level was significantly different in all groups.Fibrosis and inflamation levels decreased in ozone treatment and silver sulphadiazinegroups compared to burn+normal saline group on the 21 days according to 7 days. Inthe ozone treatment group, Glucose 6-phosphate dehydrogenase activities weresignificantly higher than the silver sulfadiazine treated group. But glutathionereductase enzyme activities were lover in the ozone treated group and hydroxyprolineconcentration decreased in ozone group compared to burn+normal saline group on 7and 21 days.Conclusions: Ozone has a detractive effect in the development of inflamation,fibrosis, and granulation via decreasing tissue damage and increasing the antioxidantenzyme activity on burn wound healing.Amaç: Ozon, hücre içinde, immüno-modülatör unsur ve antioksidan enzim işleticisinde metabolik bir uyarıcı olarak önerilmiştir. Bu çalışma, sıçanlarda yanık yarası iyileşmesinde ozon tedavisinin yararını belirlemek için yapılmıştır. Gereç ve Yöntem: Bu çalışma için 40 adet Wistar tipi sıçan 4 gruba ayrıldı: Bir kontrol grubu (yanık oluşturulmadı, bölgesel ve sistemik unsurlar kullanılmadı), bir yanık grubu (yanık oluşturuldu, ancak sadece salin verildi), bir yanık + gümüş sülfadiazin grubu (21 gün boyunca gümüş sülfadiazin uygulandı), bir yanık + ozon / oksijen karışımı grubu (21 gün boyunca ozon / oksijen karışımı uygulandı) oluşturuldu. Anestezi uygulandıktan sonra, kaynar sıcak suda (15 saniye boyunca 100 ?C) alüminyum plaka ile hayvanların sırtında ikinci derece yanık (2 cm2 alan) oluşturuldu ve kontrol grubu dışındaki diğer gruplar planlanan sürede bölgesel olarak tedavi edildi. Doku örnekleri yanık hasarından sonraki 7. ve 21. günlerde elde edildi. Doku ve kan örneklerinde biyokimyasal ve histolojik analizler yapıldı. Sonuçlar uygun istatistiksel testlerle değerlendirildi ve ± SD ortalamalar olarak verildi. Bulgular: Histopatolojik hasar düzeyi tüm gruplarda anlamlı olarak farklıydı. Ozon tedavisi ve gümüş sülfadiazin gruplarında fibroz ve inflamasyon seviyeleri, 7 güne göre 21 günde yanık + normal tuzlu su grubuna kıyasla azaldı. Ozon tedavi grubunda, Glikoz 6-fosfat dehidrogenaz aktiviteleri gümüş sülfadiazin ile tedavi edilen gruptan önemli ölçüde yüksekti. Ancak glutatyon redüktaz enzim aktiviteleri, ozon ile tedavi edilen grupta daha düşüktü ve hidroksiprolin konsantrasyonu, 7 ve 21 günde yanık + normal tuzlu su grubuna kıyasla ozon grubunda azaldı. Sonuç: Ozonun, doku hasarını azaltarak ve yanık yara iyileşmesinde antioksidan enzim aktivitesini artırarak iltihaplanma, fibrozis ve granülasyon gelişiminde bozucu bir etkisi bulunmaktadır.WOS:00061311550001

Investigation and Histopathological Evaluation of the Effects of Omeprazole on the Ischemia-Reperfusion Induced Oxidative Damage and DNA Mutation in Rat Ovarian Tissue

In this study, the biochemical and histopathological effects of omeprazole on ischemia-reperfusion (I/R) induced oxidative damage in rat ovarian tissue were investigated. The moment that the animals remained motionless in supine position was considered the appropriate time to perform surgery. The ovaries of the rats were reached through a 2.0-2.5 cm long vertical incision in the lower abdomen. Subsequently, in the omeprazole (OIR) and the control groups (I/RC), a vascular clip was placed in the lower part of the right ovary (the part where the ovary is attached to the uterus) and ischemia was maintained for 3 h. (No ischemia was applied in the healthy group.) After this period, the vascular clip was removed in order to provide reperfusion for 2 h. Afterwards, all the animals were terminated by high dose-anesthesia, the ovaries were removed and histopathological and biochemical studies were performed. Omeprazole has an antioxidant effect and it can have a protective function in the oxidative damage induced by ischemia-reperfusion. We have found that omeprazole prevents oxidative damage due to ischemia-reperfusion injury in rat ovarian tissue

Effect of thiamine pyrophosphate on ischemia-reperfusion induced oxidative damage in rat kidney

Hacimuftuoglu, Ahmet/0000-0002-9658-3313; Cetin, Nihal/0000-0003-3233-8009WOS: 000322775000005PubMed: 24014907Objectives: the biochemical effects of thiamine pyrophosphate on ischemia-reperfusion (IR) induced oxidative damage and DNA mutation in rat kidney tissue were investigated, and compared to thiamine. Materials and Methods: Rats were divided into four groups: Renal ischemia-reperfusion (RIR); thiamine pyrophosphate + RIR (TPRIR); thiamine + RIR (TRIR); and sham group (SG). Results: the results of biochemical experiments have shown that malondialdehyde (MDA) levels in rat kidney tissue after TRIR and TPRIR treatment were 7.2 +/- 0.5 (P > 0.05) and 3.3 +/- 0.3 (P 0.05), 5.8 +/- 0.4 (P 0.05), 0.93 +/- 0.1 (P < 0.0001), 0.85 +/- 0.08 (P < 0.0001), and 1.93 +/- 0.24 pmol/L, respectively. Conclusions: It has been shown that thiamine pyrophosphate prevents increase in mutagenic DNA in IR induced oxidative damage, whereas thiamine does not have this effect