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托吡酯减轻雄性大鼠主动脉夹闭诱导的肺损伤。

Topiramate Reduces Aortic Cross-Clamping-Induced Lung Injury in Male Rats.

作者信息

Kurt Aysel, Kalkan Yildiray, Turut Hasan, Cure Medine Cumhur, Tumkaya Levent, Cure Erkan

机构信息

Private Practice, Department of Thoracic Surgery, Rize, Turkey.

Private Practice, Department of Histology and Embryology, Rize, Turkey.

出版信息

Acta Medica (Hradec Kralove). 2018;61(4):144-149. doi: 10.14712/18059694.2018.133.

DOI:10.14712/18059694.2018.133
PMID:30664447
Abstract

BACKGROUND

Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R.

MATERIALS AND METHODS

A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group.

RESULTS

Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group.

CONCLUSIONS

During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.

摘要

背景

托吡酯(TPM)可减少细胞因子释放和活性氧(ROS)生成。细胞因子和内皮素-1(ET-1)分泌以及ROS形成在缺血再灌注(I/R)损伤中起重要作用。我们旨在评估TPM是否能预防I/R期间肺组织发生的损伤。

材料与方法

将27只Wistar白化大鼠分为三组,每组9只。对I/R组,通过肾下腹主动脉交叉结扎进行两小时缺血,然后进行两小时再灌注过程。TPM治疗组口服TPM(100 mg/kg/天),持续7天。在TPM治疗的最后一剂后,该组分别进行两小时缺血和两小时再灌注。

结果

TPM治疗组肺组织的肿瘤坏死因子-α(TNF-α)(p < 0.05)、丙二醛(MDA)(p < 0.05)、髓过氧化物酶(MPO)(p < 0.05)和ET-1(p < 0.05)水平显著低于I/R组。半胱天冬酶-3和组织病理学损伤也低于I/R组。

结论

在I/R期间,由于TNF-α和ET-1过度释放以及ROS生成,会发生肺损伤。TPM可通过减少细胞因子和ET-1释放以及所产生的ROS水平,很好地减轻肺损伤的发展。

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