Caffeic Acid Protects against Iron-Induced Cardiotoxicity by Suppressing Angiotensin-Converting Enzyme Activity and Modulating Lipid Spectrum, Gluconeogenesis and Nucleotide Hydrolyzing Enzyme Activities
The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO 4 . Treatment was...
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| Published in: | Biological trace element research Vol. 199; no. 3; pp. 1052 - 1061 |
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| Main Authors: | , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
New York
Springer US
01.03.2021
Springer Nature B.V |
| Subjects: | |
| ISSN: | 0163-4984, 1559-0720, 1559-0720 |
| Online Access: | Get full text |
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| Summary: | The protective effects of caffeic acid on angiotensin-converting enzyme (ACE) and purinergic enzyme activities, as well as gluconeogenesis was investigated in iron-induced cardiotoxicity. Cardiotoxicity was induced in heart tissues harvested from healthy male SD rats by 0.1 mM FeSO
4
. Treatment was carried out by co-incubating hearts tissues with caffeic acid and 0.1 mM FeSO
4
. Cardiotoxicity induction significantly (
p
< 0.05) depleted GSH level, SOD, catalase, and ENTPDase activities, with concomitant elevation of the levels of malondialdehyde (MDA), nitric oxide, ACE, ATPase, glycogen phosphorylase, glucose 6-phosphatase, fructose 6-biphsophatase, and lipase activities. There was significant (
p
< 0.05) reversion in these levels and activities on treatment with caffeic acid. Caffeic acid also caused depletion in cardiac levels of cholesterol, triglyceride, LDL-c, while elevating HDL-c level. Our results suggest the protective effect of caffeic acid against iron-mediated cardiotoxicity as indicated by its ability to suppress oxidative imbalance and ACE activity, while concomitantly modulating nucleotide hydrolysis and metabolic switch. |
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| Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
| ISSN: | 0163-4984 1559-0720 1559-0720 |
| DOI: | 10.1007/s12011-020-02227-3 |