An aqueous extract of Ammi visnaga fruits and its constituents khellin and visnagin prevent cell damage caused by oxalate in renal epithelial cells.

An aqueous extract of Ammi visnaga fruits and its constituents khellin and visnagin prevent cell damage caused by oxalate in renal epithelial cells.
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DOI:
10.1016/j.phymed.2009.10.011
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发表时间:
2010-07
期刊:
影响因子:
7.9
通讯作者:
Butterweck, V.
Butterweck, V.
中科院分区:
医学1区
文献类型:
--
作者:
Vanachayangkul, P.;Byer, K.;Khan, S.;Butterweck, V.

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从阿米visnaga L.的果实制备的茶。(syn.“Khella”)在埃及传统上被用作治疗肾结石的药物。我们研究的目的是使用LLC-PK 1和Madin-Darby-犬肾(MDCK)细胞评估Khella提取物(KE)以及两种主要成分Khellin和visnagin对肾上皮损伤的影响。这两种细胞系都提供了合适的模型系统来研究可能参与肾结石发展的细胞过程。在存在或不存在10、50、100或200 µg/mL KE的情况下,将LLC-PK 1和MDCK细胞系暴露于300 µM草酸盐(Ox)或133 µg/cm 2草酸钙一水合物(COM)。为了评价细胞损伤,通过测定乳酸脱氢酶(LDH)的释放来评估细胞活力。KE(例如100 μg/ml)显著降低LLC-PK 1(Ox:8.46± 0.76%; Ox + 100 μg/ml KE:5.41± 0.94%,p<0.001)以及MDCK细胞(Ox:30.9± 6.58%; Ox + 100 μg/ml KE:17.5± 2.50%,p<0.001)的LDH释放,这表明预防了细胞损伤。当添加COM晶体时,在两种细胞系中观察到KE的类似效果。在LLC-PK 1细胞中,khellin和visnagin均显著降低了用Ox或COM晶体预处理的细胞中的% LDH释放。然而,khellin和visnagin在MDCK细胞中表现出不同的反应。然而,在细胞暴露于Ox和COM晶体后,khellin略微降低% LDH释放,visnagin仅在COM晶体暴露后显著降低% LDH释放。总体而言,两种化合物在LLC-PK 1中比在MDCK细胞中更有活性。总之,肾上皮细胞暴露于Ox或COM晶体与LDH的显著释放相关,表明细胞损伤。我们的数据表明,KE以及khellin和visnagin可以防止由Ox和COM引起的肾上皮细胞损伤,因此可以在预防与高尿酸相关的结石形成中发挥潜在的作用。
Teas prepared from the fruits of Ammi visnaga L. (syn. “Khella”) have been traditionally used in Egypt as a remedy to treat kidney stones. It was the aim of our study to evaluate the effect of a Khella extract (KE) as well as the two major constituents khellin and visnagin on renal epithelial injury using LLC-PK1 and Madin-Darby-canine kidney (MDCK) cells. Both cell lines provide suitable model systems to study cellular processes that are possibly involved in the development of a renal stone. LLC-PK1 and MDCK cell lines were exposed to 300 µM oxalate (Ox) or 133 µg/cm2 calcium oxalate monohydrate (COM) in presence or absence of 10, 50, 100 or 200 µg/mL KE. To evaluate cell damage, cell viability was assessed by determining the release of lactate dehydrogenase (LDH). KE (e.g. 100 µg/ml) significantly decreased LDH release from LLC-PK1 (Ox: 8.46± 0.76%; Ox + 100 µg/ml KE: 5.41± 0.94%, p<0.001) as well as MDCK cells (Ox: 30.9± 6.58%; Ox + 100 µg/ml KE: 17.5± 2.50%, p<0.001), which indicated a prevention of cell damage. Similar effects for KE were observed in both cell lines when COM crystals were added. In LLC-PK1 cells khellin and visnagin both decreased the % LDH release significantly in cells that were pretreated with Ox or COM crystals. However, khellin and visnagin exhibited different responses in MDCK cells. Whereas khellin slightly reduced the % LDH release after exposure of the cells to Ox and COM crystals, visnagin significantly decreased % LDH release only after COM crystal exposure. Overall both compounds were more active in LLC-PK1 than in MDCK cells. In summary, exposure of renal epithelial cells to Ox or COM crystals was associated with a significant release of LDH indicating cell injury. Our data demonstrate that KE as well as khellin and visnagin could prevent renal epithelial cell damage caused by Ox and COM and could therefore play a potential role in the prevention of stone formation associated with hyperoxaluria.
DOI: 10.1007/s00240-002-0286-x
发表时间: 2003-03-01
影响因子: --
作者:
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发表时间: 2000-07-01
期刊: JOURNAL OF UROLOGY
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作者:
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期刊: BIOCHIMICA ET BIOPHYSICA ACTA
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发表时间: 1990-09-01
期刊: TOXICOLOGY LETTERS
影响因子: 3.5
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影响因子: 19.6
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