Gezginci-Oktayoglu Selda, Orhan Nurcan, Bolkent Sehnaz
Istanbul University, Faculty of Science, Department of Biology, 34134, Vezneciler, Istanbul, Turkey.
Istanbul University, Institute of Experimental Medicine, Department of Neuroscience, 34093, Capa, Istanbul, Turkey.
Int Immunopharmacol. 2016 Jul;36:142-150. doi: 10.1016/j.intimp.2016.04.021. Epub 2016 Apr 30.
Gastrointestinal complications are frequent in renal transplant recipients. In this regard, renal ischemia/reperfusion injury (IRI)-induced gastric damage seems to be important and there is no data available on the mechanism of this pathology. Because of its anti-inflammatory and anti-oxidant properties, it can be suggested that prostaglandin-E1 (PGE1) protects cells from renal IRI-induced gastric damage. The aim of this study was to investigate the molecular mechanisms of gastric damage induced by renal IRI and the effect of PGE1 on these mechanisms. We set an experiment with four different animal groups: physiological saline-injected and sham-operated rats, PGE1 (20μg/kg)-administered and sham operated rats, renal IRI subjected rats, and PGE1-administered and renal IRI subjected rats. The protective effect of PGE1 on renal IRI-induced gastric damage was determined based on reduced histological damage and lactate dehydrogenase activity. Moreover, we demonstrated that PGE1 shows its protective effect through reducing the production of reactive oxygen species and malondialdehyde levels. During histological examination, we observed the presence of common mononuclear cell infiltration. Therefore, pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β levels were measured and it has been shown that PGE1 suppressed both cytokines. Furthermore, it was found that PGE1 reduced the number of NF-κB(+) and caspase-3(+) inflammatory cells, and also NF-κB DNA-binding activity, while increasing proliferating cell nuclear antigen(+) epithelial cells in the stomach tissue of rats subjected to renal IR. Our data showed that PGE1 has a protective effect on renal IRI-induced oxidative stress and inflammation mediated gastric damage in rats.
胃肠道并发症在肾移植受者中很常见。在这方面，肾缺血/再灌注损伤（IRI）诱导的胃损伤似乎很重要，而且关于这种病理机制尚无可用数据。由于其抗炎和抗氧化特性，可以认为前列腺素E1（PGE1）可保护细胞免受肾IRI诱导的胃损伤。本研究的目的是探讨肾IRI诱导胃损伤的分子机制以及PGE1对这些机制的影响。我们设置了四个不同的动物组进行实验：注射生理盐水并假手术的大鼠、给予PGE1（20μg/kg）并假手术的大鼠、遭受肾IRI的大鼠以及给予PGE1并遭受肾IRI的大鼠。基于组织学损伤减轻和乳酸脱氢酶活性降低来确定PGE1对肾IRI诱导的胃损伤的保护作用。此外，我们证明PGE1通过减少活性氧的产生和丙二醛水平来发挥其保护作用。在组织学检查期间，我们观察到有常见的单核细胞浸润。因此，检测了促炎细胞因子肿瘤坏死因子-α和白细胞介素-1β的水平，结果表明PGE1可抑制这两种细胞因子。此外，发现PGE1减少了肾IRI大鼠胃组织中NF-κB(+)和caspase-3(+)炎症细胞的数量以及NF-κB的DNA结合活性，同时增加了增殖细胞核抗原(+)上皮细胞的数量。我们的数据表明，PGE1对肾IRI诱导的氧化应激和炎症介导的大鼠胃损伤具有保护作用。
