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石胆酸:氧化条件下肠道钙吸收的新型紧急保护剂。

Lithocholic acid: a new emergent protector of intestinal calcium absorption under oxidant conditions.

作者信息

Marchionatti Ana M, Pérez Adriana, Rivoira María A, Rodríguez Valeria A, Tolosa de Talamoni Nori G

机构信息

Laboratorio "Dr. Fernando Cañas", Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, INICSA (CONICET-Universidad Nacional de Córdoba), Pabellón Argentina, 2do. Piso, Ciudad Universitaria, 5000 Córdoba, Argentina.

出版信息

Biochem Cell Biol. 2017 Apr;95(2):273-279. doi: 10.1139/bcb-2016-0164. Epub 2017 Mar 20.

DOI:10.1139/bcb-2016-0164
PMID:28318299
Abstract

LCA and 1,25(OH)D are vitamin D receptor ligands with different binding affinity. The secosteroid stimulates intestinal Ca absorption. Whether LCA alters this process remains unknown. The aim of our work was to determine the effect of LCA on intestinal Ca absorption in the absence or presence of NaDOC, bile acid that inhibits the cation transport. The data show that LCA by itself did not alter intestinal Ca absorption, but prevented the inhibitory effect of NaDOC. The concomitant administration of LCA avoided the reduction of intestinal alkaline phosphatase activity caused by NaDOC. In addition, LCA blocked a decrease caused by NaDOC on gene and protein expression of molecules involved in the transcellular pathway of intestinal Ca absorption. The oxidative stress and apoptosis triggered by NaDOC were abrogated by LCA co-treatment. In conclusion, LCA placed in the intestinal lumen protects intestinal Ca absorption against the inhibitory effects caused by NaDOC. LCA avoids the reduction of the transcellular Ca movement, apparently by blocking the oxidative stress and apoptosis triggered by NaDOC, normalizing the gene and protein expression of molecules involved in Ca movement. Therefore, LCA might become a possible treatment to improve intestinal calcium absorption under oxidant conditions.

摘要

LCA和1,25(OH)D是具有不同结合亲和力的维生素D受体配体。这种甾体化合物能刺激肠道对钙的吸收。LCA是否会改变这一过程尚不清楚。我们这项研究的目的是确定在存在或不存在NaDOC(一种抑制阳离子转运的胆汁酸)的情况下,LCA对肠道钙吸收的影响。数据表明,LCA本身不会改变肠道钙吸收,但能阻止NaDOC的抑制作用。同时给予LCA可避免由NaDOC引起的肠道碱性磷酸酶活性降低。此外,LCA阻止了NaDOC对参与肠道钙吸收跨细胞途径的分子的基因和蛋白质表达的降低。LCA共同处理可消除由NaDOC引发的氧化应激和细胞凋亡。总之,置于肠腔内的LCA可保护肠道钙吸收免受NaDOC引起的抑制作用。LCA避免了跨细胞钙转运的减少,显然是通过阻断由NaDOC引发的氧化应激和细胞凋亡,使参与钙转运的分子的基因和蛋白质表达正常化。因此,LCA可能成为在氧化条件下改善肠道钙吸收的一种可能的治疗方法。

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