实验性恶唑酮诱导大鼠结肠炎中芳烃受体和ATG16L1蛋白的表达。

Zherebiatiev As, Kamyshny Am
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引用次数: 1

摘要

我们研究了实验性恶唑酮诱导大鼠结肠炎中AhR和ATG16L1蛋白的表达以及IL-1受体重组拮抗剂(ARIL-1)和辛伐他汀的抗炎作用。采用单克隆大鼠抗体间接免疫荧光法测定免疫阳性细胞。结肠炎的发生伴随着结肠淋巴组织中atg16l1淋巴细胞总数的增加(30%,P < 0.05)。而AhR(+)-淋巴细胞的数量没有变化。同时使免疫阳性细胞中ATG16L1蛋白浓度升高4-11%,P < 0.05。在实验病理发展过程中给予辛伐他汀和ARIL-1可使结肠AhR(+)总数减少24-38% (P < 0.05), ATG16L1(+)-淋巴细胞总数减少43% - 2倍(P < 0.05)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Expression of aryl hydrocarbon receptor and ATG16L1 protein in experimental oxazolone-induced colitis in rats.
We studied the expression of AhR and ATG16L1 protein in experimental oxazolone-induced colitis in rats and anti-inflammatory action of recombinant antagonist of IL-1 receptors (ARIL-1) and simvastatin. The immunopositive cells were determined using an indirect immunofluorescence technique with using a monoclonal rat antibody. It has been established that development of colitis was accompanied by an increase of total number of ATG16L1-lymphocytes (by 30%, P < 0.05) in lymphoid structures of the colon. However the amount of AhR(+)-lymphocytes has not changed. At the same time has increased the concentration of ATG16L1 protein (by 4-11%, P < 0.05) in immunopositive cells. Administration of simvastatin and ARIL-1 during the development of experimental pathology was accompanied by decrease of total number of AhR(+) (by 24-38%, P < 0.05) and ATG16L1(+)-lymphocytes (by 43% - 2 fold, P < 0.05) in the colon.
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