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Vitamin A prevents lipopolysaccharide‐induced injury on tight junctions in mice

机译:维生素A可防止脂多糖诱导的小鼠紧密交叉点损伤

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Vitamin A (VA) is one of the most widely used food supplements, but its molecular mechanisms largely remain elusive. Previously, we have demonstrated that VA inhibits the action of lipopolysaccharide (LPS) on intestinal epithelial barrier function and tight junction proteins using IPEC‐J2 cells, one of representative intestinal cell lines as a cellular model. These exciting findings stimulated us continue to determine the effects of VA on LPS‐induced damage of intestinal integrity in mice. Our results demonstrated that LPS treatment caused reductions of the mRNA levels of tight junction proteins including Zo‐1, Occludin, and Claudin‐1, well‐known biomarkers of intestinal integrity, and these reductions were reversed by VA pretreatment. Intestinal immunofluorescent results of Claudin‐1 revealed that LPS disrupted the structure of tight junction and reduced the expression of Claudin‐1 at protein level, which was reversed by VA pretreatment. These results suggest that VA may exert a profound role on preventing intestinal inflammation in vivo.
机译:维生素A(VA)是最广泛使用的食品补充剂之一,但其分子机制在很大程度上仍然难以实现。以前,我们已经证明VA抑制脂多糖(LPS)对肠上皮阻挡函数和使用IPEC-J2细胞的紧密接线蛋白的作用,作为蜂窝模型的代表性肠细胞系之一。这些令人兴奋的结果刺激了美国继续确定VA对小鼠肠道完整性损伤的影响。我们的结果表明,LPS处理引起了ZO-1,Occludin和Claudin-1,肠道完整性众所周知的生物标志物,肠道内蛋白质的mRNA水平降低,并且通过VA预处理逆转了这些减少。 Claudin-1的肠道免疫荧光结果显示,LPS扰乱了紧密结的结构,并降低了蛋白质水平的克劳丁-1的表达,其被VA预处理逆转。这些结果表明,VA可能对预防体内肠道炎症产生深远的作用。

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