trans-Cinnamaldehyde mitigated intestinal inflammation induced by Cronobacter sakazakii in newborn mice
trans-Cinnamaldehyde mitigated intestinal inflammation induced by Cronobacter sakazakii in newborn mice
复制标题
反式肉桂醛减轻新生小鼠坂崎克罗诺杆菌诱导的肠道炎症
DOI：
10.1039/c9fo00410f
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发表时间：
2019-05-01
期刊：
影响因子：
6.1
通讯作者：
Shi, Chao
中科院分区：
文献类型：
--
作者：
Yang, Gaoji;Jin, Tong;Shi, Chao
坏死性小肠结肠炎（NEC）是一种严重的肠道疾病，与新生儿的高死亡率（40-60%）相关。坂崎恶势力是NEC的一个重要因素。然而，关于NEC的发病机制和治疗方法的研究仍然有限。给你，C。采用坂崎制作的小鼠新生期肠道炎症模型，观察反式肉桂醛（TC）对感染的影响。TC处理使C.抑制回肠组织中坂崎肠杆菌的集落形成单位，减轻肠组织的形态学损伤。此外，它减少了感染C.坂崎。此外，TC处理抑制caspase-3活性，调节肠上皮细胞凋亡，并抑制核因子-κ B信号通路激活由C。坂崎。提示TC对C.因此，本发明的目的是提供一种预防NEC的潜在药物。
Necrotizing enterocolitis (NEC) is a serious intestinal disease associated with a high mortality (40-60%) in newborn infants. Cronobacter sakazakii is an important factor for NEC. However, studies regarding NEC pathogenesis and therapeutic treatments are still limited. Here, a C. sakazakii-induced mouse neonatal intestinal inflammation model was employed to determine the effects of trans-cinnamaldehyde (TC) on infections. TC treatment reduced the number of C. sakazakii colony-forming units in the ileal tissues and mitigated the morphological damage in intestinal tissues. Additionally, it reduced the mRNA transcription of inflammatory genes and production of interleukin 6 and tumor necrosis factor- in mice infected with C. sakazakii. Moreover, TC treatment suppressed caspase-3 activity, modulated enterocyte apoptosis, and inhibited the nuclear factor-kappa B signaling pathway activation induced by C. sakazakii. These findings suggest that TC has protective effects on C. sakazakii-induced murine intestinal inflammation and that it may be a potential agent for preventing NEC.