PDF(Pubmed)
Abstract：
UNASSIGNED: Cisplatin is one of the most frequently used chemotherapeutics, which is known to cause both tumor and normal lung tissue damage through the generation of free radicals and cells apoptosis/necrosis. Melatonin is a neurohormone that regulates numerous physiological processes in the body both through receptor pathways and by maintaining tissue redox homeostasis.
UNASSIGNED: The extent of rat lung damage induced by cisplatin and the effects of melatonin on this process was determined based on the pathohistological changes and biochemical disturbances in tissue lipid peroxidation, protein carbonyl modification and in the activity of xanthine oxidase (XO), caspase-3 and DNases.
UNASSIGNED: Histopathological analysis of rat lung tissue obtained from animals that received cisplatin found them to be edematous, with significant deterioration of alveolar epithelium. These morphological changes are accompanied by a significant increase in all studied oxidative stress-related parameters, as well as with the activity of apoptosis-related enzymes. A five-day treatment with melatonin completely prevented a cisplatin-induced increase in oxidative stress-related parameters and in the activity of XO, caspase-3 and alkaline DNase. Also, the histopathological changes observed during microscopic analysis were much less pronounced than in the group that received cisplatin only.
UNASSIGNED: These results can potentially be connected with the ability of melatonin to inhibit the activity of XO, caspase-3 and alkaline DNase and/or its ability to scavenge free radicals, thus preventing lung damage induced by cisplatin.
UNASSIGNED: The extent of rat lung damage induced by cisplatin and the effects of melatonin on this process was determined based on the pathohistological changes and biochemical disturbances in tissue lipid peroxidation, protein carbonyl modification and in the activity of xanthine oxidase (XO), caspase-3 and DNases.
UNASSIGNED: Histopathological analysis of rat lung tissue obtained from animals that received cisplatin found them to be edematous, with significant deterioration of alveolar epithelium. These morphological changes are accompanied by a significant increase in all studied oxidative stress-related parameters, as well as with the activity of apoptosis-related enzymes. A five-day treatment with melatonin completely prevented a cisplatin-induced increase in oxidative stress-related parameters and in the activity of XO, caspase-3 and alkaline DNase. Also, the histopathological changes observed during microscopic analysis were much less pronounced than in the group that received cisplatin only.
UNASSIGNED: These results can potentially be connected with the ability of melatonin to inhibit the activity of XO, caspase-3 and alkaline DNase and/or its ability to scavenge free radicals, thus preventing lung damage induced by cisplatin.
摘要：
■顺铂是最常用的化疗药物之一，已知其通过产生自由基和细胞凋亡/坏死而引起肿瘤和正常肺组织损伤。褪黑素是一种神经激素，它通过受体途径和维持组织氧化还原稳态来调节体内的许多生理过程。
■顺铂诱导的大鼠肺损伤程度和褪黑素对该过程的影响是根据组织脂质过氧化的病理组织学变化和生化紊乱确定的，蛋白质羰基修饰和黄嘌呤氧化酶（XO）的活性，caspase-3和DNA酶。
■从接受顺铂的动物获得的大鼠肺组织的组织病理学分析发现它们是水肿的，肺泡上皮显著恶化。这些形态学变化伴随着所有研究的氧化应激相关参数的显着增加，以及凋亡相关酶的活性。用褪黑激素治疗五天完全阻止了顺铂诱导的氧化应激相关参数和XO活性的增加，caspase-3和碱性DNA酶。此外，在显微镜分析中观察到的组织病理学变化远不及仅接受顺铂治疗的组。
■这些结果可能与褪黑激素抑制XO活性的能力有关，caspase-3和碱性DNA酶和/或其清除自由基的能力，从而防止顺铂引起的肺损伤。
■顺铂诱导的大鼠肺损伤程度和褪黑素对该过程的影响是根据组织脂质过氧化的病理组织学变化和生化紊乱确定的，蛋白质羰基修饰和黄嘌呤氧化酶（XO）的活性，caspase-3和DNA酶。
■从接受顺铂的动物获得的大鼠肺组织的组织病理学分析发现它们是水肿的，肺泡上皮显著恶化。这些形态学变化伴随着所有研究的氧化应激相关参数的显着增加，以及凋亡相关酶的活性。用褪黑激素治疗五天完全阻止了顺铂诱导的氧化应激相关参数和XO活性的增加，caspase-3和碱性DNA酶。此外，在显微镜分析中观察到的组织病理学变化远不及仅接受顺铂治疗的组。
■这些结果可能与褪黑激素抑制XO活性的能力有关，caspase-3和碱性DNA酶和/或其清除自由基的能力，从而防止顺铂引起的肺损伤。
