Zainumi Cut Meliza, Siregar Gontar Alamsyah, Wijaya Dadik Wahyu, Ichwan Muhammad
Department of Anesthesiology and Intensive Care, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia.
Department of Internal Medicine, Faculty of Medicine, Universitas Sumatera Utara, Medan, Indonesia.
Heliyon. 2022 Aug 18;8(8):e10236. doi: 10.1016/j.heliyon.2022.e10236. eCollection 2022 Aug.
Sepsis is a major cause of death in intensive care units whose development is supported by an imbalance of oxidative stress and antioxidant. (SOD) is a primer endogen antioxidant that prevents (ROS). Extensive studies on animals and humans have examined L.C, a cantaloupe rich in SOD, and its combination with . The studies aimed to determine the effect of enteral administration of L.C. gliadin (CME-gliadin) 28 days before inducing sepsis in rats. This experimental study aimed to compare four groups of male Wistar rats, including negative and positive control rats and those supplemented with SOD CME-gliadin 1 IU/day and SOD CME-gliadin 5 IU/day. All rats were given the same standard, except the supplementation for 28 days. Sepsis was induced by intraperitoneal injection of LPS 10 mg/kg. Enteral administration of SOD - gliadin extract of CME-gliadin for 28 days was used as antioxidant prophylaxis against oxidative stress due to sepsis. The results showed that enteral administration of CME-gliadin of 1 IU/day and 5 IU/day significantly increased SOD levels based on examination after 14 and 28 days. Also, it significantly decreased MDA (p < 0.001), TNF-α (p < 0.001), and lactate levels in rats induced by sepsis. However, the increase in lactate levels was above >1.64 mmol/l, indicating a high mortality rate. There was no significant difference in SOD, MDA, TNF-α, and Lactate levels between SOD 1 IU and SOD 5 IU. This descriptive data show that SOD 5 IU has a better result in MDA, TNF-α, and Lactate levels than SOD 1 IU.
脓毒症是重症监护病房患者死亡的主要原因,其发展受到氧化应激和抗氧化剂失衡的影响。超氧化物歧化酶(SOD)是一种主要的内源性抗氧化剂,可预防活性氧(ROS)。针对动物和人类进行了大量研究,研究了富含SOD的哈蜜瓜L.C及其与其他物质的组合。这些研究旨在确定在大鼠诱导脓毒症前28天经肠给予L.C.麦醇溶蛋白(CME-麦醇溶蛋白)的效果。本实验研究旨在比较四组雄性Wistar大鼠,包括阴性和阳性对照大鼠以及补充1 IU/天和5 IU/天SOD CME-麦醇溶蛋白的大鼠。除了28天的补充剂外,所有大鼠都给予相同的标准饮食。通过腹腔注射10 mg/kg LPS诱导脓毒症。经肠给予CME-麦醇溶蛋白的SOD - 麦醇溶蛋白提取物28天,用作针对脓毒症引起的氧化应激的抗氧化预防措施。结果显示,基于14天和28天后的检查,经肠给予1 IU/天和5 IU/天的CME-麦醇溶蛋白可显著提高SOD水平。此外,它还显著降低了脓毒症诱导的大鼠体内的丙二醛(p < 0.001)、肿瘤坏死因子-α(p < 0.001)和乳酸水平。然而,乳酸水平的升高超过>1.64 mmol/l,表明死亡率很高。SOD 1 IU和SOD 5 IU之间的SOD、丙二醛、肿瘤坏死因子-α和乳酸水平没有显著差异。这些描述性数据表明,SOD 5 IU在丙二醛、肿瘤坏死因子-α和乳酸水平方面比SOD 1 IU有更好的结果。