NDLI: The oxygen radical generator pyrogallol impairs cardiomyocyte contractile function via a superoxide and p38 MAP kinase-dependent pathway : Protection by anisodamine and tetramethylpyrazine

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The oxygen radical generator pyrogallol impairs cardiomyocyte contractile function via a superoxide and p38 MAP kinase-dependent pathway : Protection by anisodamine and tetramethylpyrazine

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The oxygen radical generator pyrogallol impairs cardiomyocyte contractile function via a superoxide and p38 MAP kinase-dependent pathway : Protection by anisodamine and tetramethylpyrazine

Content Provider	Springer Nature Link
Author	Esberg, Lucy B. Ren, Jun
Copyright Year	2004
Abstract	Oxygen-derived free radicals have been demonstrated to contribute to the pathogenesis of myocardial dysfunction, although the underlying mechanism remains not fully understood. This study was designed to examine the role of the superoxide generator pyrogallol on cardiac contractile function and possible intervention with herbal medicines anisodamine and tetramethylpyrazine (TMP) on pyrogallol-induced cardiac contractile response. Adult rat ventricular myocytes were isolated and stimulated to contract at 0.5 Hz. Mechanical properties were evaluated using an lonOptix system including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR$_{90}$), and maximal velocity of shortening/relengthening (±dL/dt). A 10-min exposure of pyrogallol (0 to 10$^{−2}$ M) did not affect cardiac contractile mechanics. However, longer duration of pyrogallol exposure (1, 3, and 6 h) significantly shortened resting cell length, reduced PS and ±dL/dt, and prolonged TPS and TR$_{90}$ in time- and concentration-dependent manners. The pyrogallol (10$^{−4}$ M with 6-h incubation)-induced mechanical defects were prevented by the p38 mitogen-activated protein (MAP) kinase inhibitor SB203580 (1 μM) and superoxide dismutase (SOD, 500 U/mL) with the exception that pyrogallol-induced PS depression was unaffected by SOD. Interestingly, incubation of herbal antioxidants anisodamine (10$^{−7}$ M) and TMP (10$^{−7}$ M) effectively attenuated the pyrogallol-induced cardiac mechanical defects with the exception of PS unaffected by TMP. Our data demonstrate a direct inhibitory effect of pyrogallol on cardiac contraction, probably in a superoxide- and p38 MAP kinase-dependent manner. The antioxidant medicines anisodamine and TMP may be useful in the treatment of oxygen free radical-induced myocardial dysfunction.
Starting Page	375
Ending Page	384
Page Count	10
File Format	PDF
ISSN	15307905
Journal	Cardiovascular Toxicology
Volume Number	4
Issue Number	4
e-ISSN	15590259
Language	English
Publisher	Humana Press
Publisher Date	2004-01-01
Publisher Place	Totowa
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Pyrogallol p38 MAP kinase anisodamine tetramethylpyrazine myocyte shortening Pharmacology/Toxicology Cardiology
Content Type	Text
Resource Type	Article
Subject	Molecular Biology Toxicology Cardiology and Cardiovascular Medicine

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