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Effects of taurine and Astragalus membranaceus on ion currents and their expression in cardiomyocytes after CVB3 infection
Author(s) -
Su YanGang,
Yang YingZhen,
Bao WeiSheng,
Liu GongXin,
Ge Jun Bo,
Chen Haozhu
Publication year - 2003
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.10130
Subject(s) - taurine , astragalus , potassium channel , chemistry , protein subunit , collagenase , calcium channel , in vivo , endocrinology , microbiology and biotechnology , medicine , pharmacology , calcium , biology , biochemistry , enzyme , pathology , amino acid , traditional chinese medicine , gene , alternative medicine
To investigate the effects of taurine and Astragalus membranaceus (AM) on ion currents and their expression in cardiomyocytes after Coxsackie virus B3 (CVB3) infection, hearts were removed from adult or newborn Sprague‐Dawley rats and digested by collagenase. CVB3 was inoculated to the medium and used for recording current of L‐type voltage‐dependent calcium channel ( I ca ), Na + current ( I Na ), outward potassium current ( I out ), and inward rectifying potassium current ( I KI ). An in vivo model of viral myocarditis (VMC) was produced by intraperitoneal injection of CVB3 into BALB/c mice and the hearts were used for examining the expression of L‐type voltage‐dependent Ca 2+ channel (LVDCC)α1 subunit and the voltage‐gated potassium channel (Kv). I ca and I out were increased while I KI decreased after inoculation with CVB3 for 2 h. However, I Na did not differ between normal and infected cells. The positive hybridization signals of the LVDCCα1 subunit (antigen) and Kv1.2, Kv2.1, and Kv4.2 were much reinforced after CVB3 infection. Taurine and AM could block the enhancement of I ca , I out , and reduction of I KI after virus infection. Additionally, taurine and AM attenuated the increased expression level of LVDCCα1 subunit as well as Kv mRNA. Taurine and AM may exert their beneficial effect on VMC through modulating the changes in ion currents and expression. Drug Dev. Res. 58:57–60, 2003. © 2003 Wiley‐Liss, Inc.