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The relation of oxidative stress and apoptosis to histopathologic alterations in the lungs as a result of global cerebral ischemia.
Biotechnic & Histochemistry ( IF 1.6 ) Pub Date : 2019-08-03 , DOI: 10.1080/10520295.2019.1601768
H Yeşil 1 , I Tuğlu 2
Affiliation  

Heart attack and oxygen deficiency may cause necrosis in the brain and other tissues. We investigated the histopathological effects of nitric oxide (NO) on ischemia/reperfusion in lung and hippocampus using a rat brain bilateral occlusion ischemia model. Male rats were assigned to sham (SH), ischemic preconditioning (PC), global ischemia (GI) and ischemic reperfusion (IR) groups. Before ischemia was induced, blood was drawn to induce hypovolemic hypotension and for blood gas testing. After sacrifice, samples of hippocampus were harvested. Sections were examined using hematoxylin and eosin (H & E) staining and immunostaining using primary antibodies for GFAP, S100β, iNOS, eNOS and the TUNEL method. Following ischemia, we found evidence of gliosis induced oxidative stress and apoptosis in the hippocampus. No significant differences were detected between the SH and PC groups. In the GI and IR groups, apoptosis and necrosis were observed in the hippocampus. Lung sections were stained with H & E and Masson's trichrome (MT) and immunostained for iNOS and eNOS. The TUNEL method was used to detect apoptosis. Interstitial edema, vascular congestion, intra-alveolar hemorrhage, perivascular edema, neutrophil infiltration and disruption of alveoli were observed after global ischemia and ischemic reperfusion. Inflammatory cells were detected in the connective tissue. The IR and GI groups exhibited significantly more apoptotic cells than the SH or PC groups. Free radicals, such as nitric oxide (NO), that appear following ischemia and reperfusion in the brain may also injure the lungs. Increased NO in both lung and brain tissue suggests that apoptosis in these organs can be induced by reactive nitrogen species.

中文翻译:

氧化应激和细胞凋亡与全脑缺血导致的肺组织病理改变的关系。

心脏病发作和缺氧可能导致大脑和其他组织坏死。我们使用大鼠脑双侧闭塞缺血模型调查了一氧化氮(NO)对肺和海马缺血/再灌注的组织病理学影响。雄性大鼠分为假手术(SH),缺血预处理(PC),整体缺血(GI)和缺血再灌注(IR)组。在诱发缺血之前,抽取血液以诱发低血容量性低血压并进行血气检测。处死后,收获海马样品。使用苏木精和曙红(H&E)染色检查切片,并使用GFAP,S100β,iNOS,eNOS和TUNEL方法的一抗进行免疫染色。缺血后,我们发现神经胶质增生引起海马氧化应激和细胞凋亡的证据。SH组和PC组之间未发现明显差异。在GI和IR组中,在海马中观察到凋亡和坏死。肺切片用H&E和Masson's trichrome(MT)染色,并对iNOS和eNOS进行免疫染色。TUNEL法用于检测细胞凋亡。在整体缺血和局部缺血再灌注后,观察到间质性水肿,血管充血,肺泡内出血,血管周水肿,中性粒细胞浸润和肺泡破坏。在结缔组织中检测到炎性细胞。IR和GI组比SH或PC组显示出更多的凋亡细胞。脑缺血和再灌注后出现的自由基,例如一氧化氮(NO)也可能伤害肺。
更新日期:2019-11-01
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