Abstract:

Diclofenac (DF) is among non-steroidal anti-inflammatory drugs and in high doses it has toxic effects on various tissues, including the heart. Chrysin (CRS) has many beneficial effects such as antioxidant and anti-apoptotic. In the present study, the effects of CRS on DF-induced cardiotoxicity were investigated. For this purpose, after DF and/or CRS treatments were applied to Sprague Dawley rats, the markers of oxidative stress, endoplasmic reticulum stress and apoptosis in heart tissues and serum CK-MB levels were analyzed. The data obtained displayed that oxidative stress induced by DF was alleviated by triggering the expression of SOD, CAT and GPx enzymes and increasing GSH levels after CRS administration, and a decrease in MDA levels occurred. It was also determined that the expressions of ATF-6, PERK, IRE1 and GRP78, which are ER stress markers and induced by DF, were downregulated after CRS treatment. Additionally, CRS suppressed Bax and Caspase-3 expressions and increased Bcl-2 expression in connection with ER stress. Another finding of this study demonstrated that CK-MB levels, which are an important indicator of heart damage, decreased after CRS administration. As a result, CRS provided a significant protection against cardiotoxicity caused by DF.

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