Koç Alparslan, Kuyrukluyildiz Ufuk, Gazi Mustafa, Caner Sayar Ali, Altuner Durdu, Süleyman Halis, Yavuzer Bülent, Abdulkadir Çoban Taha, Süleyman Zeynep, Naz Yazici Gülce
Department of Anesthesiology and Reanimation, Erzincan Binali Yildirim University Mengucek Gazi Training and Research Hospital, Basbaglar District, Erzincan, Turkey.
Gen Physiol Biophys. 2023 Jan;42(1):67-75. doi: 10.4149/gpb_2022049.
The primary sources of reactive oxygen species (ROS) that cause ischemia-reperfusion (I/R) injuries are enzymes xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate oxidases (NOXs) in the literature, whereby one of the main ROS producing cells via NOX activity are polymophonuclear leukocytes (PNL). Sugammadex, the effect of which we plan to research against gastric I/R damage, is a modified gamma-cyclodextrin that antagonizes the action of steroidal neuromuscular blocking drugs. Previous studies have reported that sugammadex inhibits PNL infiltration. However, it is unknown whether an inhibitory effect on XO is present. We aimed to biochemically and histopathologically investigate the effects of sugammadex on I/R-induced stomach damage in rats. The animals were divided into groups that underwent gastric ischemia-reperfusion (GIR), 4 mg/kg sugammadex + gastric ischemia-reperfusion (SGIR), and a sham operation group (SG). The effect of sugammadex was evaluated by measuring oxidant-antioxidant and PNL parameters. There was no significant difference in XO levels between the SGIR and GIR groups. In the SGIR group, sugammadex inhibited the increase in myeloperoxidase (MPO) and malondialdehyde (MDA) levels (p < 0.001). The amount of MDA and MPO in the SGIR group was similar as in the SG group. Sugammadex significantly suppressed the decrease in tGSH levels in the SGIR group (p < 0.001). The difference between tGSH levels in the SG and SGIR groups was slight. In the SGIR group, sugammadex significantly suppressed the increase in tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL1-β) levels compared to the GIR group (p < 0.001). Additionally, sugammadex corrected histopathological modifications as much as sham group. In conclusion, sugammadex may be beneficial in preventing oxidative stress.
文献中指出，导致缺血再灌注（I/R）损伤的活性氧（ROS）的主要来源是黄嘌呤氧化酶（XO）和烟酰胺腺嘌呤二核苷酸磷酸氧化酶（NOXs），其中通过NOX活性产生ROS的主要细胞之一是多形核白细胞（PNL）。我们计划研究其对胃I/R损伤影响的舒更葡糖钠是一种修饰的γ-环糊精，可拮抗甾体神经肌肉阻滞药物的作用。先前的研究报道舒更葡糖钠可抑制PNL浸润。然而，其对XO是否具有抑制作用尚不清楚。我们旨在通过生物化学和组织病理学方法研究舒更葡糖钠对大鼠I/R诱导的胃损伤的影响。将动物分为经历胃缺血再灌注（GIR）组、4mg/kg舒更葡糖钠+胃缺血再灌注（SGIR）组和假手术组（SG）。通过测量氧化-抗氧化参数和PNL参数来评估舒更葡糖钠的作用。SGIR组和GIR组之间的XO水平无显著差异。在SGIR组中，舒更葡糖钠抑制了髓过氧化物酶（MPO）和丙二醛（MDA）水平的升高（p<0.001）。SGIR组中MDA和MPO的量与SG组相似。舒更葡糖钠显著抑制了SGIR组中总谷胱甘肽（tGSH）水平的降低（p<0.001）。SG组和SGIR组之间的tGSH水平差异很小。在SGIR组中，与GIR组相比，舒更葡糖钠显著抑制了肿瘤坏死因子α（TNF-α）和白细胞介素1β（IL1-β）水平的升高（p<0.001）。此外，舒更葡糖钠使组织病理学改变恢复到与假手术组一样的程度。总之，舒更葡糖钠可能对预防氧化应激有益。
