Sun Mao-Cheng, Hou Ping-Ping, Wang Xin-Yu, Zhao Chang-Hui, Cheng Bi-Jun, Wang Yan-Ling, Hao Hong-Wei, Zhang Tie-Hua, Ye Hai-Qing
College of Food Science and Engineering, Jilin University, Changchun, China.
School of Public Health, Jilin Medical University, Jilin City, China.
Food Nutr Res. 2018 Oct 29;62. doi: 10.29219/fnr.v62.1469. eCollection 2018.
Previous studies suggested that probiotics intervention may be one of the methods for preventing and/or treating gastric ulcer.
The aim of the study was to compare the preventive effects of a spaceflight mutant F-9-35 and its wild type on ethanol-induced gastric injury in rats.
Forty rats were randomly allocated into five groups: a normal group (NOR), ethanol group (EtOH), skim milk group (MILK), F-9-35 group (F935) and wild-type group (WT). The NOR and EtOH groups received 1 ml of distilled water by daily gavage for 14 days. The MILK group received 1 ml of skim milk alone, while the F935 and WT groups were administered 1 ml of skim milk containing the mutant and wild type (1 × 10 colony-forming unit/ml) by daily gavage for 14 days, respectively. Acute gastric injury was induced by absolute alcohol 1 h after the final administration of different treatments, except for the NOR group.
Pretreatment with F-9-35, but not milk alone or milk with the wild type, showed significant reduction of ethanol-induced gastric injury, as evidenced by lowering of ulcer index, ulcer area (%), and histological lesion. F-9-35 decreased the levels of lipid peroxidation and myeloperoxidase and increased mucus, glutathione, and nitric oxide levels in gastric tissue. Moreover, F-9-35 inhibited the expression of proinflammatory genes including gastric tumor necrosis factor-α, interleukin-1β, and cyclooxygenase-2 and decreased the activity of nuclear factor kappa B (NF-κB).
These findings indicated that F-9-35 pretreatment can attenuate ethanol-induced gastric injury in rats by inhibiting oxidative stress and inflammatory response. Together, F-9-35 has potential preventive efficacy on gastric ulcer.
先前的研究表明,益生菌干预可能是预防和/或治疗胃溃疡的方法之一。
本研究旨在比较航天诱变菌株F-9-35及其野生型对大鼠乙醇诱导的胃损伤的预防作用。
将40只大鼠随机分为五组:正常组(NOR)、乙醇组(EtOH)、脱脂牛奶组(MILK)、F-9-35组(F935)和野生型组(WT)。NOR组和EtOH组每天经口灌胃1 ml蒸馏水,共14天。MILK组单独给予1 ml脱脂牛奶,而F935组和WT组分别每天经口灌胃1 ml含诱变菌株和野生型(1×10菌落形成单位/ml)的脱脂牛奶,共14天。除NOR组外,在末次给予不同处理1 h后,用无水乙醇诱导急性胃损伤。
用F-9-35预处理可显著减轻乙醇诱导的胃损伤,而单独使用牛奶或牛奶与野生型联合使用则无此效果,这可通过溃疡指数、溃疡面积(%)和组织学损伤的降低得以证明。F-9-35降低了胃组织中脂质过氧化和髓过氧化物酶的水平,并增加了黏液、谷胱甘肽和一氧化氮的水平。此外,F-9-35抑制了包括胃肿瘤坏死因子-α、白细胞介素-1β和环氧化酶-2在内的促炎基因的表达,并降低了核因子κB(NF-κB)的活性。
这些发现表明,F-9-35预处理可通过抑制氧化应激和炎症反应减轻大鼠乙醇诱导的胃损伤。总之,F-9-35对胃溃疡具有潜在的预防作用。