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The effect of ellagic acid on caspase-3/bcl-2/Nrf-2/NF-kB/TNF-α /COX-2 gene expression product apoptosis pathway: a new approach for muscle damage therapy
The goal of this study was to determine the protective role of ellagic acid (EA) against CCl 4 -induced muscle injury in rats. In this study, 36 Wistar albino rats (n = 36, 8 weeks old) were used. The rats were divided into 4 groups and 9 rats were included each group. Groups: (i) control Group: sta...
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Published in: | Molecular biology reports 2020-04, Vol.47 (4), p.2573-2582 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The goal of this study was to determine the protective role of ellagic acid (EA) against CCl
4
-induced muscle injury in rats. In this study, 36 Wistar albino rats (n = 36, 8 weeks old) were used. The rats were divided into 4 groups and 9 rats were included each group. Groups: (i) control Group: standard diet; (ii) EA Group: standard diet + EA group; (iii) CCl
4
group: standard diet + CCl
4
group; (iv) EA + CCl
4
group: standard diet + EA + CCl
4
. The animals were decapitated after 8 weeks, and their muscle tissues were received and investigated. In the muscle tissue, TNF-α, COX-2, Nrf-2, NF-kB, caspase-3 and bcl-2 expression levels were analyzed by the western blotting technique, lipid peroxidation was detected by MDA (malondialdehyde), and catalase and GSH levels were determined by a spectrophotometer. In our findings, in comparison to the CCl
4
group, in the EA + CCl
4
group, the Nrf-2 and caspase-3 protein expression levels, GSH and catalase activities increased, while the NF-kB, bcl-2, TNF-α and COX-2 protein expression levels and MDA levels decreased. These results suggest that EA reduces muscle tissue damage rate in rats and that EA may also be used as a potential drug to protect against muscle tissue damage in the future.
Graphic abstract |
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ISSN: | 0301-4851 1573-4978 |
DOI: | 10.1007/s11033-020-05340-7 |