Wang Fang-Yan, Liu Jia-Ming, Luo Hai-Hua, Liu Ai-Hua, Jiang Yong
Fang-Yan Wang, Hai-Hua Luo, Ai-Hua Liu, Yong Jiang, State Key Laboratory of Organ Failure Research, Nanfang Hospital, Guangzhou 510515, Guangdong Province, China.
World J Gastroenterol. 2015 Jul 21;21(27):8340-51. doi: 10.3748/wjg.v21.i27.8340.
To investigate the effects of Clostridium butyricum (C. butyricum) on experimental gastric ulcers (GUs) induced by alcohol, restraint cold stress, or pyloric ligation in mice, respectively.
One hundred and twenty mice were randomly allocated into three types of gastric ulcer models (n = 40 each), induced by alcohol, restraint cold stress, or pyloric ligation. In each GU model, 40 mice were allocated into four groups (n = 10 each): the sham control group; model group (GU induction without pretreatment); C. butyricum group (GU induction with C. butyricum pretreatment); and Omeprazole group (GU induction with Omeprazole pretreatment). The effects of C. butyricum were evaluated by examining the histological changes in the gastric mucosal erosion area, the activities of superoxide dismutase (SOD) and catalase (CAT), the level of malondialdehyde (MDA), and the contents of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, leukotriene B4 (LTB4) and 6-keto-PGF-1α (degradation product of PGI2) in the gastric tissue.
Our data showed that C. butyricum significantly reduced the gastric mucosal injury area and ameliorated the pathological conditions of the gastric mucosa. C. butyricum not only minimized the decreases in activity of SOD and CAT, but also reduced the level of MDA in all three GU models used in this study. The accumulation of IL1-β, TNF-α and LBT4 decreased, while 6-keto-PGF-1α increased with pretreatment by C. butyricum in all three GU models.
Our data demonstrated the protective effects of pretreatment with C. butyricum on anti-oxidation and anti-inflammation in different types of GU models in mice. Further studies are needed to explore its potential clinical benefits.
分别研究丁酸梭菌对酒精、束缚冷应激或幽门结扎诱导的小鼠实验性胃溃疡的影响。
将120只小鼠随机分为三种胃溃疡模型(每种模型40只),分别由酒精、束缚冷应激或幽门结扎诱导。在每种胃溃疡模型中,40只小鼠再分为四组(每组10只):假手术对照组;模型组(未预处理诱导胃溃疡);丁酸梭菌组(用丁酸梭菌预处理诱导胃溃疡);奥美拉唑组(用奥美拉唑预处理诱导胃溃疡)。通过检查胃黏膜糜烂面积的组织学变化、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的活性、丙二醛(MDA)水平以及胃组织中白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、白三烯B4(LTB4)和6-酮-前列腺素F-1α(前列环素I2的降解产物)的含量来评估丁酸梭菌的作用。
我们的数据表明,丁酸梭菌显著减少了胃黏膜损伤面积,改善了胃黏膜的病理状况。在本研究使用的所有三种胃溃疡模型中,丁酸梭菌不仅使SOD和CAT活性的降低最小化,还降低了MDA水平。在所有三种胃溃疡模型中,经丁酸梭菌预处理后,IL-1β、TNF-α和LBT4的积累减少,而6-酮-前列腺素F-1α增加。
我们的数据证明了丁酸梭菌预处理对小鼠不同类型胃溃疡模型的抗氧化和抗炎保护作用。需要进一步研究以探索其潜在的临床益处。