Laboratory of Translational Physiology and Pharmacology, Pharmaceutical Sciences Graduate Program, Vila Velha University (UVV), Vila Velha, ES, Brazil.
Laboratory of Translational Physiology and Pharmacology, Pharmaceutical Sciences Graduate Program, Vila Velha University (UVV), Vila Velha, ES, Brazil.
Life Sci. 2018 Sep 15;209:370-376. doi: 10.1016/j.lfs.2018.08.035. Epub 2018 Aug 16.
This study investigated the gastroprotective effects and the systemic oxidative status of oral kefir pretreatment in albino mice submitted to acute gastric ulcer induced by indomethacin.
Male Swiss mice were divided into three groups (n = 7): Vehicle (0.3 mL of whole milk/100 g body weight, pH adjusted to 5.0), Kefir (0.3 mL of kefir/100 g body weight) and Proton Pump Inhibitor (PPI, 30 mg/kg of lansoprazole), via gavage for 14 days. Animals were fasted for 16 h and treated orally with indomethacin (40 mg/kg). After 6 h the animals were euthanized, the blood samples were obtained and used for the determination of ROS production, oxidation of macromolecules and apoptosis. The stomachs were removed, opened by the greater curvature, and a macroscopic analysis of the gastric lesions was performed.
Our findings demonstrated that the symbiotic kefir significantly alleviated blood oxidative stress by reducing superoxide anion, hydrogen peroxide and hydroxyl/peroxynitrite radicals, thereby leading to reduced oxidative damage to macromolecules due to a decreased oxidative stress status in induced gastric lesions. These anti-oxidative properties might contribute favorably to the ulcer attenuation in the kefir group.
Taken together, these findings support a significant role played by the antioxidant actions of kefir in counteracting the gastric damage induced by this cyclooxygenase inhibitor. It is also worthy to mention that, kefir also exerted the gastroprotective property partly by inhibiting oxidative systemic damage. Based on these considerations, it was implied that kefir might be a contributor for the ROS-scavenging effect.
本研究旨在探讨口服克菲尔预处理对吲哚美辛诱导的急性胃溃疡的白老鼠的胃保护作用和全身氧化状态。
雄性瑞士老鼠被分为三组（n=7）：载剂（0.3 毫升全脂牛奶/100 克体重，pH 值调至 5.0）、克菲尔（0.3 毫升克菲尔/100 克体重）和质子泵抑制剂（PPI，30 毫克/公斤兰索拉唑），通过灌胃 14 天。动物禁食 16 小时，口服吲哚美辛（40 毫克/公斤）。6 小时后，处死动物，采集血液样本，用于测定 ROS 生成、大分子氧化和细胞凋亡。取出胃，沿大弯剪开，对胃损伤进行宏观分析。
我们的研究结果表明，共生克菲尔通过减少超氧阴离子、过氧化氢和羟基/过氧亚硝酸盐自由基，显著缓解了血液氧化应激，从而降低了诱导性胃损伤中大分子的氧化损伤，因为氧化应激状态降低。这些抗氧化特性可能有利于克菲尔组溃疡的减轻。
综上所述，这些发现支持了克菲尔的抗氧化作用在对抗这种环氧化酶抑制剂引起的胃损伤方面的重要作用。值得一提的是，克菲尔还通过抑制氧化系统损伤发挥了胃保护作用。基于这些考虑，暗示了克菲尔可能是 ROS 清除作用的贡献者。
