Background:Ischemia–reperfusion injury (IRI) poses a significant challenge for physicians, necessitating the management of cell damage and the preservation of organ functions. Various surgical procedures, such as vascular surgery on extremities, temporary cross-clamping of the abdominal aorta in aortic surgery, and the use of a tourniquet in extremity surgeries, may induce lower limb IRI. The susceptibility to IRI is heightened in individuals with diabetes. This study aimed to investigate the effects of fullerenol C60 and sevoflurane on mouse muscle tissue in a lower limb IRI model and to assess their potential in preventing complications arising from ischemia–reperfusion in mice with streptozocin-induced diabetes.Methods:A total of 36 adult Swiss albino mice were randomly divided into six groups, each consisting of six mice: control group (group C), diabetes group (group D), diabetes–ischemia/reperfusion group (group DIR), diabetes–ischemia/reperfusion–fullerenol C60 group (group DIR-FC60), diabetes–ischemia/reperfusion–sevoflurane group (group DIR-S), and diabetes–ischemia/reperfusion–sevoflurane–fullerenol C60 group (DIR-S-FC60). Streptozocin (55 mg/kg) was intraperitoneally administered to induce diabetes in the relevant groups, with mice displaying blood glucose levels of 250 mg/dL or higher at 72 h were considered diabetic. After 4 weeks, all groups underwent laparotomy under anesthesia. In DIR-FC60 and DIR-S-FC60 groups, fullerenol C60 (100 mg/kg) was intraperitoneally administrated 30 min before the ischemia period. Sevoflurane, delivered in 100% oxygen at a rate of 2.3% and 4 L/min, was administered during the ischemia period in DIR-S and DIR-S-FC60 groups. In the IR groups, a microvascular clamp was placed on the infrarenal abdominal aorta for 120 min during the ischemia period, followed by the removal of the clamp and a 120-min reperfusion period. At the end of the reperfusion, gastrocnemius muscle tissues were removed for histopathological and biochemical parameter examinations.Results:Histopathological examination revealed a significant reduction in the disorganization and degeneration of muscle cells in the DIR-S-FC60 group compared to the DIR group (p = 0.041). Inflammatory cell infiltration was notably lower in the DIR-S, DIR-FC60, and DIR-S-FC60 groups than in the DIR group (p = 0.031, p = 0.011, and p = 0.013, respectively). The total damage scores in the DIR-FC60 and DIR-S-FC60 groups were significantly lower than in the DIR group (p = 0.018 and p = 0.008, respectively). Furthermore, the levels of malondialdehyde (MDA) in the DIR-S, DIR-FC60, and DIR-S-FC60 groups were significantly lower than in the DIR group (p < 0.001, p < 0.001, and p < 0.001, respectively). Catalase (CAT) enzyme activity in the DIR-S, DIR-FC60, and DIR-S-FC60 groups was higher than in the DIR group (p = 0.001, p = 0.014, and p < 0.001, respectively). Superoxide dismutase (SOD) enzyme activity in the DIR-FC60 and DIR-S-FC60 groups was also higher than in the DIR group (p < 0.001 and p = 0.001, respectively).Conclusion:Our findings indicate that administering fullerenol C60 30 min prior to ischemia in diabetic mice, in combination with sevoflurane, led to a reduction in oxidative stress and the correction of IR-related damage in muscle tissue histopathology. We believe that the administration of fullerenol C60 before IR, coupled with sevoflurane administration during IR, exerts a protective effect in mice.

中文翻译：

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七氟烷和富勒醇C60对链佐星糖尿病小鼠下肢缺血再灌注损伤的影响

背景：缺血再灌注损伤（IRI）给医生带来了重大挑战，需要处理细胞损伤和保护器官功能。各种外科手术，例如四肢血管手术、主动脉手术中腹主动脉的临时交叉夹紧以及四肢手术中使用止血带，都可能诱发下肢IRI。糖尿病患者对 IRI 的易感性更高。本研究旨在研究富勒烯醇 C60 和七氟烷对下肢 IRI 模型中小鼠肌肉组织的影响，并评估它们在预防链佐星诱导糖尿病小鼠缺血再灌注并发症方面的潜力。方法：总共 36 名成年小鼠瑞士白化小鼠随机分为六组，每组六只小鼠：对照组（C组）、糖尿病组（D组）、糖尿病-缺血/再灌注组（DIR组）、糖尿病-缺血/再灌注-富勒烯醇C60组(DIR-FC60组)、糖尿病-缺血/再灌注-七氟醚组(DIR-S组)和糖尿病-缺血/再灌注-七氟醚-富勒烯醇C60组(DIR-S-FC60)。腹腔注射链脲佐菌素（55 mg/kg）诱导相关组糖尿病，72小时血糖水平为250 mg/dL或更高的小鼠被认为患有糖尿病。 4周后，所有组均在麻醉下接受剖腹手术。在DIR-FC60和DIR-S-FC60组中，在缺血期前30分钟腹腔内给予富勒醇C60（100mg/kg）。 DIR-S 和 DIR-S-FC60 组在缺血期间以 2.3% 和 4 L/min 的速率在 100% 氧气中输送七氟烷。在IR组中，在缺血期间将微血管夹放置在肾下腹主动脉上120分钟，然后移除夹子并进行120分钟的再灌注期。再灌注结束时，取出腓肠肌组织进行组织病理学和生化参数检查。结果：组织病理学检查显示，与DIR组相比，DIR-S-FC60组肌细胞的解体和变性明显减少（p = 0.041）。 DIR-S、DIR-FC60 和 DIR-S-FC60 组的炎症细胞浸润明显低于 DIR 组（分别为 p = 0.031、p = 0.011 和 p = 0.013）。 DIR-FC60 和 DIR-S-FC60 组的总损伤评分显着低于 DIR 组（分别为 p = 0.018 和 p = 0.008）。此外，DIR-S、DIR-FC60 和 DIR-S-FC60 组的丙二醛 (MDA) 水平显着低于 DIR 组（分别为 p < 0.001、p < 0.001 和 p < 0.001） 。 DIR-S、DIR-FC60 和 DIR-S-FC60 组的过氧化氢酶 (CAT) 酶活性高于 DIR 组（分别为 p = 0.001、p = 0.014 和 p < 0.001）。DIR-FC60 和 DIR-S-FC60 组的超氧化物歧化酶 (SOD) 酶活性也高于 DIR 组（分别为 p < 0.001 和 p = 0.001）。结论：我们的研究结果表明，给予富勒烯醇 C60 30 分钟在糖尿病小鼠缺血之前，与七氟醚联合使用，可以减少氧化应激并纠正肌肉组织病理学中与IR相关的损伤。我们相信，在 IR 之前给予富勒烯醇 C60，再加上 IR 期间给予七氟醚，可以对小鼠产生保护作用。