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Cardiovascular Toxicology

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01.12.2013

Inhibitory Effect of Gallic Acid on Advanced Glycation End Products Induced Up-Regulation of Inflammatory Cytokines and Matrix Proteins in H9C2 (2-1) Cells

verfasst von: Subramanian Umadevi, Venkatachalam Gopi, Elangovan Vellaichamy

Erschienen in: Cardiovascular Toxicology | Ausgabe 4/2013

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Abstract

Accumulating evidences have demonstrated that increased production of advanced glycation end products (AGEs) contributes to etiology of cardiac complications in diabetes. However, the underlying mechanism of AGE-induced effects is not well understood. Recent studies evince the beneficial role of phytochemicals in reducing the risk of cardiovascular morbidity and mortality in patients with cardiovascular diseases and diabetes mellitus. Hence, in the present study, the cardio protective role of gallic acid (GA) against in vitro synthesized AGE in H9C2 (2-1) cells was elucidated. H9C2 (2-1) cells exposed to AGE (100 μg/ml) with/without GA pre-treatment (10 μM) and the release of reactive oxygen species (ROS), expression of oxidative stress markers, matrix proteins, and cytokines were analyzed. Cells exposed to AGE demonstrate a significant increase in ROS release with augmented expression (P < 0.01) of receptor for AGE (RAGE) and NOX-p47 phox (P < 0.001) proteins compared to untreated control cells. Moreover, an increased expression of matrix proteins and cytokines such as TNF-α (P < 0.01), TGF-β (P < 0.001), and iNOS (P < 0.001) was also found in AGE-treated cells, whereas, cells pre-treated with N-acetyl cysteine or RAGE neutralizing antibody notably (P < 0.01) impede the ROS release. Further, cells pre-treated with GA significantly attenuated the expression of NOX, RAGE, and other cytokines. In addition, the abnormal expressions of matrix proteins were also decreased especially in GA-treated cells. Thus, the results of the present study demonstrated the deleterious effect of AGEs that directly induce oxidative stress and matrix derangement and, on the other way, the “pleiotropic” activity of GA in reducing the risk of AGE-mediated cellular complications.

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Titel: Inhibitory Effect of Gallic Acid on Advanced Glycation End Products Induced Up-Regulation of Inflammatory Cytokines and Matrix Proteins in H9C2 (2-1) Cells
verfasst von: Subramanian Umadevi
Venkatachalam Gopi
Elangovan Vellaichamy
Publikationsdatum: 01.12.2013
Verlag: Springer US
Erschienen in: Cardiovascular Toxicology / Ausgabe 4/2013
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI: https://doi.org/10.1007/s12012-013-9222-2

Springer Medizin

Abstract

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