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BACKGROUND: This study aims to investigate the effects of blunt lung trauma performed in experimental rat model on lung tissue and blood as well as proinflammatory cytokines, oxidant-antioxidant enzymes and histopathological parameters after Ngamma-nitro-L-arginine methyl ester and N-iminoethyl-L-ornithine administration. METHODS: The study included 50 adult male Wistar albino rats (weighing 350 to 400 g). Rats were randomly allocated into four groups. Except in the control, moderate-level pulmonary contusion was created in all other groups. Intraperitoneal saline solution was performed in groups 1 and 2, 25 mg.kg-1 Ngamma-nitro-L-arginine methyl ester in group 3, and 20 mg.kg-1 N-iminoethyl-L-ornithine in group 4. Blood and lung tissues were studied biochemically and histopathologically. RESULTS: Best outcomes were recorded statistically significantly in groups with administration of Ngamma-nitro-L-arginine methyl ester and N-iminoethyl-L-ornithine when malondialdehyde response, mucous and histopathological values were examined. Significant improvement was detected in superoxide dismutase values in the group with administration of competitive nitric oxide synthase inhibitor Ngamma-nitro-L-arginine methyl ester. Nitric oxide values were substantially decreased in N-iminoethyl-L-ornithine group, while no significance was detected. CONCLUSION: Free oxygen radicals and lipid peroxidation played a role in pulmonary contusion after blunt lung trauma. According to biochemical and histopathological outcomes, effects of inflammation were decreased and protective effects were formed with administration of both Ngammanitro- L-arginine methyl ester and N-iminoethyl-L-ornithine.
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BACKGROUND: This study aims to compare clopidogrel and rivaroxaban against ischemia-reperfusion injury after a long reperfusion time and to investigate its effects on various tissues. METHODS: A total of 40 Wistar rats were included in the study and were randomly divided into four groups (n=10 per group). Groups were defined as follows: control (Group 1), sham (Group 2), clopidogrel pre-treatment (Group 3), and rivaroxaban pre-treatment (Group 4). Ischemia (6 h) and reperfusion (8 h) were induced at the lower hind limb in Groups 2, 3, and 4. The ischemic muscle, heart, kidney, liver, and plasma tissues of the subjects were obtained to test for the oxidant (malondialdehyde) and antioxidants (glutathione, superoxide dismutase, and nitric oxide). RESULTS: Malondialdehyde levels were significantly higher in the sham group, compared to the controls in all tissues. Clopidogrel and rivaroxaban pre-treatment significantly decreased malondialdehyde levels, compared to the heart, ischemic muscle, liver, and blood tissues of the sham group. Kidney malondialdehyde levels were reduced only by rivaroxaban. Group 4 had significantly decreased malondialdehyde levels, compared to Group 3 in ischemic muscle (p<0.010). The glutathione reduction, compared to sham group, in the kidney was only significant for Group 4 (p<0.050). With clopidogrel and rivaroxaban pretreatment, nitric oxide levels significantly decreased only in the heart tissue, compared to sham group (p<0.001 and p<0.050, respectively). CONCLUSION: The study results suggest that rivaroxaban and clopidogrel are effective in reducing ischemia-reperfusion injury in the heart, ischemic muscle, liver, and blood. Rivaroxaban also protects the kidneys and is superior to clopidogrel in ischemic muscle protection.
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OBJECTIVE: Cisplatin (DDP, cis-diamminedichloroplatinium II) is one of the most potent chemotherapeutic antitumor drugs, but is able to generate reactive oxygen species (ROS) and it also inhibits the activity of antioxidant enzymes in renal tissue. In the present study, we investigated the preventive effect of 100, 200 and 400 mg/kg b.w. doses of vitamin E (VE), and 25, 50, and 100 mg/kg b.w. doses of vitamin A (VA) combination on malondialdehyde (MDA), nitric oxide (NO), and glutathione (GSH) levels and superoxide dismutase (SOD) activity in cisplatin-induced toxicity in rat kidneys. Our literature survey indicated a lack of any experimental study showing the beneficial effect of VA on cisplatin-induced MDA, NO, GSH and SOD changes. For this reason, we hoped that this study would provide a unique contribution in that respect. MATERIALS AND METHODS: 59 Wistar rats (11 to replace prematurely lost animals) were used. 48 evaluable rats were divided into 8 groups (n = 6 in each group): control group, DDP alone (5 mg/kg b.w.) group, 3 VE combination treatment groups of VE100+DDP, VE200+DDP, and VE400+DDP, and 3 VA combination treatment groups of VA25+DDP, VA50+DDP, and VA100+DDP. Kidney MDA, GSH, NO levels and SOD activities were determined for the assessment of oxidant-antioxidant balance. RESULTS: While in the DDP group the tissue levels of MDA and NO were found to be significantly higher than in the control group, GSH levels and SOD activities were significantly lower. MDA and NO levels were found to be significantly lower and GSH levels and SOD activities significantly higher in the VE200+DDP and VE400+ DDP groups when compared with the DDP alone group. MDA and NO levels were found to be significantly lower in the VA50+DDP and VA100+DDP groups when compared with the DDP alone group. However, identical comparisons with the DDP alone group showed significantly higher GSH levels and SOD activities in the VA25+DDP, VA50+DDP, and VA100+DDP groups. Among the VE100+ DDP, VE200+DDP, and VE400+DDP groups, and VA25+ DDP, VA50+DDP, and VA100+DDP groups, MDA and NO levels decreased and GSH levels and SOD activities increased steadily and significantly as the doses of VE and VA increased. CONCLUSION: These vitamins would be effective in protecting against cisplatin-induced tissue damage in rat kidneys. It is possible that the toxic effect of cisplatin is somehow minimized by a compensatory mechanism involving VE and VA via induction of antioxidant enzyme activities following intraperitoneal injection of DDP.
