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氧化铈对远距离器官损伤实验性心肌缺血再灌注模型中肾脏和肝脏组织损伤的影响。

Effects of Cerium Oxide on Kidney and Liver Tissue Damage in an Experimental Myocardial Ischemia-Reperfusion Model of Distant Organ Damage.

作者信息

Güneş Işın, Dursun Ali Doğan, Özdemir Çağrı, Küçük Ayşegül, Sezen Şaban Cem, Arslan Mustafa, Özer Abdullah

机构信息

Department of Anesthesiology and Reanimation, Erciyes University Faculty of Medicine, Kayseri 38039, Turkey.

Department of Physiology, Atılım University Faculty of Medicine, Ankara 06560, Turkey.

出版信息

Medicina (Kaunas). 2024 Dec 11;60(12):2044. doi: 10.3390/medicina60122044.

DOI:10.3390/medicina60122044
PMID:39768923
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11728079/
Abstract

Ischemia-reperfusion (I/R) injury is a process in which impaired perfusion is restored by restoring blood flow and tissue recirculation. Nanomedicine uses cutting-edge technologies that emerge from interdisciplinary influences. In the literature, there are very few in vivo and in vitro studies on how cerium oxide (CeO) affects systemic anti-inflammatory response and inflammation. Therefore, in our study, we aimed to investigate whether CeO administration has a protective effect against myocardial I/R injury in the liver and kidneys. Twenty-four rats were randomly divided into four groups after obtaining approval from an ethics committee. A control (group C), cerium oxide (group CO), IR (group IR), and Cerium oxide-IR (CO-IR group) groups were formed. Intraperitoneal CeO was administered at a dose of 0.5 mg/kg 30 min before left thoracotomy and left main coronary (LAD) ligation, and myocardial muscle ischemia was induced for 30 min. After LAD ligation was removed, reperfusion was performed for 120 min. All rats were euthanized using ketamine, and blood was collected. Liver and kidney tissue samples were evaluated histopathologically. Serum AST (aspartate aminotransferase), ALT (alanine aminotransaminase), GGT (gamma-glutamyl transferase), glucose, TOS (), and TAS () levels were also measured. Necrotic cell and mononuclear cell infiltration in the liver parenchyma of rats in the IR group was observed to be significantly increased compared to the other groups. Hepatocyte degeneration was greater in the IR group compared to groups C and CO. Vascular vacuolization and hypertrophy, tubular degeneration, and necrosis were increased in the kidney tissue of the IR group compared to the other groups. Tubular dilatation was significantly higher in the IR group than in the C and CO groups. TOS was significantly higher in all groups than in the IR group ( < 0.0001, < 0.0001, and = 0.006, respectively). However, TAS level was lower in the IR group than in the other groups ( = 0.002, = 0.020, and = 0.031, respectively). Renal and liver histopathological findings decreased significantly in the CO-IR group compared to the IR group. A decrease in the TOS level and an increase in the TAS level were found compared to the IR group. The AST, ALT, GGT, and Glucose levels are shown. CeO administered before ischemia-reperfusion reduced oxidative stress and ameliorated IR-induced damage in distant organs. We suggest that CeO exerts protective effects in the myocardial IR model.

摘要

缺血再灌注(I/R)损伤是一个通过恢复血流和组织再循环来恢复受损灌注的过程。纳米医学采用源于跨学科影响的前沿技术。在文献中,关于氧化铈(CeO)如何影响全身抗炎反应和炎症的体内和体外研究非常少。因此,在我们的研究中,我们旨在研究给予CeO是否对肝脏和肾脏的心肌I/R损伤具有保护作用。在获得伦理委员会批准后,将24只大鼠随机分为四组。形成了对照组(C组)、氧化铈组(CO组)、I/R组(IR组)和氧化铈-I/R组(CO-IR组)。在左胸切开术和左冠状动脉前降支(LAD)结扎前30分钟,以0.5mg/kg的剂量腹腔注射CeO,并诱导心肌缺血30分钟。去除LAD结扎后,进行120分钟的再灌注。所有大鼠使用氯胺酮安乐死,并采集血液。对肝脏和肾脏组织样本进行组织病理学评估。还测量了血清天冬氨酸氨基转移酶(AST)、丙氨酸氨基转移酶(ALT)、γ-谷氨酰转移酶(GGT)、葡萄糖、总氧化应激(TOS)和总抗氧化能力(TAS)水平。与其他组相比,IR组大鼠肝实质中的坏死细胞和单核细胞浸润明显增加。与C组和CO组相比,IR组的肝细胞变性更大。与其他组相比,IR组肾脏组织中的血管空泡化和肥大、肾小管变性和坏死增加。IR组的肾小管扩张明显高于C组和CO组。所有组的TOS均显著高于IR组(分别为P<0.0001、P<0.0001和P = 0.006)。然而,IR组的TAS水平低于其他组(分别为P = 0.002、P = 0.020和P = 0.031)。与IR组相比,CO-IR组的肾脏和肝脏组织病理学结果显著降低。与IR组相比,发现TOS水平降低,TAS水平升高。显示了AST、ALT、GGT和葡萄糖水平。在缺血再灌注前给予CeO可降低氧化应激并改善远处器官的I/R诱导损伤。我们认为CeO在心肌I/R模型中发挥保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b44/11728079/c5a24d98d18a/medicina-60-02044-g013.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b44/11728079/2b0086b25961/medicina-60-02044-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7b44/11728079/df8b81ccf9c3/medicina-60-02044-g009.jpg
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