F. Şahin, M. Orhan, A. Tas Tuna, Onur Palabıyık, Nevcihan ŞAHUTOĞLU BAL, S. I. Gözükara, Ö. Budak, H. Cakiroglu
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Malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) enzyme levels were performed the lung tissue and tissues were examined histopathologically. \nResult: A significant difference was found between the groups in terms of MDA, SOD, CAT levels (respectively; p < 0.001, p=0.008, p < 0.001). A significant difference was found between the groups in terms of lung tissue neutrophil/lymphocyte infiltration scores and alveolar wall thickening scores (respectively p=0.009, p=0.002). \nConclusion: The biochemical and histopathological results of the present study suggested that amantadine, like other NMDA antagonist agents, may have a protective effect on lung tissues against the damage caused by hepatic I/R injury. Although we observed significant improvements after the administration of both doses studied, there was no significant difference between these two doses in terms of their success in protecting against distant organ lung injury. Amantadine appears promising as a therapeutic agent in treatment.","PeriodicalId":174708,"journal":{"name":"Konuralp Tıp Dergisi","volume":"1 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2022-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Effect of Different Doses of Amantadine on Lung Tissue In Hepatıc Ischemia Reperfusion Injury in Rats\",\"authors\":\"F. Şahin, M. Orhan, A. Tas Tuna, Onur Palabıyık, Nevcihan ŞAHUTOĞLU BAL, S. I. Gözükara, Ö. Budak, H. Cakiroglu\",\"doi\":\"10.18521/ktd.1161896\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective: N-Methyl D-Aspartate (NMDA) receptor blockers have been shown to have protective effects against ischemia/reperfusion (I/R) injury in various tissues. The aim of this study was to investigate the effects of 90 ve 135 mg/kg doses of amantadine on lung in hepatic I/R injury. \\nMethod: The rats were randomly divided into six groups: Group Sham, Group I/R, Group Amantadine-90, Group Amantadine-135, Group I/R-90 and Group I/R-135. In I/R, an atraumatic vascular clamp was applied to the structures in the left portal triad for 45 minutes and reperfusion period was 2 hours after ischemia. Malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) enzyme levels were performed the lung tissue and tissues were examined histopathologically. \\nResult: A significant difference was found between the groups in terms of MDA, SOD, CAT levels (respectively; p < 0.001, p=0.008, p < 0.001). A significant difference was found between the groups in terms of lung tissue neutrophil/lymphocyte infiltration scores and alveolar wall thickening scores (respectively p=0.009, p=0.002). \\nConclusion: The biochemical and histopathological results of the present study suggested that amantadine, like other NMDA antagonist agents, may have a protective effect on lung tissues against the damage caused by hepatic I/R injury. Although we observed significant improvements after the administration of both doses studied, there was no significant difference between these two doses in terms of their success in protecting against distant organ lung injury. 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引用次数: 0
摘要
目的:n -甲基d -天冬氨酸(NMDA)受体阻滞剂对多种组织缺血/再灌注(I/R)损伤具有保护作用。本研究旨在探讨金刚烷胺90mg /kg和135mg /kg剂量对肝I/R损伤肺的影响。方法:将大鼠随机分为6组:Sham组、I/R组、金刚烷胺90组、金刚烷胺135组、I/R-90组和I/R-135组。在I/R中,在缺血后再灌注2小时,在左门静脉三联结构上应用无创性血管钳45分钟。检测肺组织丙二醛(MDA)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)水平,并进行组织病理学检查。结果:各组间MDA、SOD、CAT水平(分别为;P < 0.001, P =0.008, P < 0.001)。两组间肺组织中性粒细胞/淋巴细胞浸润评分和肺泡壁增厚评分差异有统计学意义(p=0.009, p=0.002)。结论:本研究的生化和组织病理学结果表明,金刚烷胺与其他NMDA拮抗剂一样,可能对肝I/R损伤的肺组织有保护作用。虽然我们观察到在两种剂量的治疗后都有显著的改善,但在保护远端器官肺损伤方面,这两种剂量之间没有显著差异。金刚烷胺是一种很有前途的治疗药物。
The Effect of Different Doses of Amantadine on Lung Tissue In Hepatıc Ischemia Reperfusion Injury in Rats
Objective: N-Methyl D-Aspartate (NMDA) receptor blockers have been shown to have protective effects against ischemia/reperfusion (I/R) injury in various tissues. The aim of this study was to investigate the effects of 90 ve 135 mg/kg doses of amantadine on lung in hepatic I/R injury.
Method: The rats were randomly divided into six groups: Group Sham, Group I/R, Group Amantadine-90, Group Amantadine-135, Group I/R-90 and Group I/R-135. In I/R, an atraumatic vascular clamp was applied to the structures in the left portal triad for 45 minutes and reperfusion period was 2 hours after ischemia. Malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) enzyme levels were performed the lung tissue and tissues were examined histopathologically.
Result: A significant difference was found between the groups in terms of MDA, SOD, CAT levels (respectively; p < 0.001, p=0.008, p < 0.001). A significant difference was found between the groups in terms of lung tissue neutrophil/lymphocyte infiltration scores and alveolar wall thickening scores (respectively p=0.009, p=0.002).
Conclusion: The biochemical and histopathological results of the present study suggested that amantadine, like other NMDA antagonist agents, may have a protective effect on lung tissues against the damage caused by hepatic I/R injury. Although we observed significant improvements after the administration of both doses studied, there was no significant difference between these two doses in terms of their success in protecting against distant organ lung injury. Amantadine appears promising as a therapeutic agent in treatment.