دورية أكاديمية
Investigation of effect of tectorigenin (O-methylated isoflavone) on Ca2+ signal transduction and cytotoxic responses in canine renal tubular cells
| العنوان: | Investigation of effect of tectorigenin (O-methylated isoflavone) on Ca2+ signal transduction and cytotoxic responses in canine renal tubular cells |
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| المؤلفون: | He-Hsiung Cheng, Wei-Zhe Liang, Wei-Chuan Liao, Chun-Chi Kuo, Lyh-Jyh Hao, Chiang-Ting Chou, Chung-Ren Jan |
| المصدر: | Chinese Journal of Physiology, Vol 63, Iss 2, Pp 60-67 (2020) |
| بيانات النشر: | Wolters Kluwer Medknow Publications, 2020. |
| سنة النشر: | 2020 |
| المجموعة: | LCC:Physiology |
| مصطلحات موضوعية: | ca2+ signal transduction, madin-darby canine kidney, tectorigenin, viability, Physiology, QP1-981 |
| الوصف: | Tectorigenin, a traditional Chinese medicine, is isolated from the flower of plants such as Pueraria thomsonii Benth. It is an O-methylated isoflavone, a type of flavonoid. Previous studies have shown that tectorigenin evoked various physiological responses in different models, but the effect of tectorigenin on cytosolic-free Ca2+ levels ([Ca2+]i) and cytotoxicity in renal tubular cells is unknown. Our research explored if tectorigenin changed Ca2+ signal transduction and viability in Madin–Darby Canine Kidney (MDCK) renal tubular cells. [Ca2+]i in suspended cells were measured by applying the fluorescent Ca2+-sensitive probe fura-2. Viability was explored by using water-soluble tetrazolium-1 as a fluorescent dye. Tectorigenin at concentrations of 5–50 μM induced [Ca2+]i rises. Ca2+ removal reduced the signal by approximately 20%. Tectorigenin (50 μM) induced Mn2+ influx suggesting of Ca2+ entry. Tectorigenin-induced Ca2+ entry was inhibited by 10% by three inhibitors of store-operated Ca2+ channels, namely, nifedipine, econazole, and SKF96365. In Ca2+-free medium, treatment with the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin inhibited 83% of tectorigenin-evoked [Ca2+]i rises. Conversely, treatment with tectorigenin abolished thapsigargin-evoked [Ca2+]i rises. Inhibition of phospholipase C with U73122 inhibited 50% of tectorigenin-induced [Ca2+]i rises. Tectorigenin at concentrations between 10 and 60 μM killed cells in a concentration-dependent fashion. Chelation of cytosolic Ca2+ with 1,2-bis (2-aminophenoxy)ethane-N, N, N', N'-tetraacetic acid/acetoxy methyl did not reverse tectorigenin's cytotoxicity. Our data suggest that, in MDCK cells, tectorigenin evoked [Ca2+]i rises and induced cell death that was not associated with [Ca2+]i rises. Therefore, tectorigenin may be a Ca2+-independent cytotoxic agent for kidney cells. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 0304-4920 2666-0059 |
| Relation: | http://www.cjphysiology.org/article.asp?issn=0304-4920;year=2020;volume=63;issue=2;spage=60;epage=67;aulast=Cheng; https://doaj.org/toc/0304-4920; https://doaj.org/toc/2666-0059 |
| DOI: | 10.4103/CJP.CJP_14_20 |
| URL الوصول: | https://doaj.org/article/dbacada934f14cc2bfc31d7d8713ce4b |
| رقم الأكسشن: | edsdoj.bacada934f14cc2bfc31d7d8713ce4b |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 03044920 26660059 |
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| DOI: | 10.4103/CJP.CJP_14_20 |