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- Title
Effect of tetramethylpyrazine (TMP) on Ca<sup>2+</sup> signal transduction and cell viability in a model of renal tubular cells.
- Authors
Fang, Yi‐Chien; Chou, Chiang‐Ting; Liang, Wei‐Zhe; Kuo, Chun‐Chi; Hsu, Shu‐Shong; Wang, Jue‐Long; Jan, Chung‐Ren
- Abstract
Tetramethylpyrazine (TMP) is a compound purified from herb. Its effect on Ca2+ concentrations ([Ca2+]i) in renal cells is unclear. This study examined whether TMP altered Ca2+ signaling in Madin-Darby canine kidney (MDCK) cells. TMP at 100-800 μM induced [Ca2+]i rises, which were reduced by Ca2+ removal. TMP induced Mn2+ influx implicating Ca2+ entry. TMP-induced Ca2+ entry was inhibited by 30% by modulators of protein kinase C (PKC) and store-operated Ca2+ channels. Treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) inhibited 93% of TMP-evoked [Ca2+]i rises. Treatment with TMP abolished BHQ-evoked [Ca2+]i rises. Inhibition of phospholipase C (PLC) abolished TMP-induced responses. TMP at 200-1000 μM decreased viability, which was not reversed by pretreatment with the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid-acetoxymethyl ester. Together, in MDCK cells, TMP induced [Ca2+]i rises by evoking PLC-dependent Ca2+ release from endoplasmic reticulum and Ca2+ entry via PKC-sensitive store-operated Ca2+ entry. TMP also caused Ca2+-independent cell death.
- Publication
Journal of Biochemical & Molecular Toxicology, 2017, Vol 31, Issue 10, pn/a
- ISSN
1095-6670
- Publication type
Article
- DOI
10.1002/jbt.21952