Abstract：
:Iron-mediated oxidative stress has been recognized as one of the leading causes of chronic kidney injury. The effect of L-type calcium channel (LTCC) blocker on iron overload has been shown in cardiomyocytes, liver cells, and nerve cells. So far, few studies have examined whether blockers improve kidney iron-mediated oxidative stress. Yet, the precise mechanism through which blockers regulate kidney iron transport still remains unclear. In the present work, treatment with nifedipine or verapamil decreased oxidative stress and reduced the cell apoptosis-induced by ferric ammonium citrate (P < 0.05), decreased cellular iron contents, and prevented the rising of iron level-induced by ferric ammonium citrate (P > 0.05) in HK-2 and HEK293 cells. Besides, nifedipine and verapamil treatments increased the expression of divalent metal transporter 1, divalent metal transporter ZIP14, and ferroportin1 in HK-2 cells and increased ferroportin1 expression in HEK293 cells. In summary, LTCC blockers alleviate iron overload-induced oxidative stress in renal epithelial cells by blocking the iron uptake and enhancing cellular iron transport and/or iron export, thus synergistically reducing the cellular iron accumulation. Consequently, LTCC blockers may be used as a novel treatment for the prevention of primary or secondary iron overload-kidney injury.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Sun L,Lin X,Pornprasert S,Lü X,Ran B,Lin Ydoi
10.1016/j.ejphar.2020.173513subject
Has Abstractpub_date
2020-11-05 00:00:00pages
173513eissn
0014-2999issn
1879-0712pii
S0014-2999(20)30605-1journal_volume
886pub_type
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