| Aims: Cisplatin (CPL) is a potent chemotherapeutic agent widely used to treat various cancers. However, CPL causes toxicity in various tissues, including the heart. Lipoic acid (LPA) is a thiol compound with antioxidant, anti-inflammatory, and antiapoptotic properties. Although LPA has been reported to have protective effects in various cardiac diseases, the mechanisms underlying its cardio-protective effects have not been elucidated. This study aimed to establish a CPL-induced cardiotoxicity model in the H9c2 cardiomyocyte cell line, to understand the mechanisms underlying this cardiotoxicity, and to investigate the effect of LPA on cardiotoxicity.Methods: H9c2 cardiomyocyte cells as control (CNT), CPL (40 μm), and LPA-1 (300 μm LPA, and 40 μm CPL), LPA-2 (500 μm LPA, and 40 μm CPL) in combination along with CIS were used. In the analyses made, glutathione (GSH) and glutathione peroxidase (GSHPx) enzyme activity, lipid peroxidation [malondialdehyde,(MDA)] levels, inflammation markers interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α levels, total oxidant/antioxidant (TOS and TAS) status levels, reactive oxygen species (ROS) and caspase activity (Casp 3 and 9) in the cells were determined. Results: CIS treatment caused cardiomyocyte cell toxicity and increased Casp 3, Casp 9, ROS, IL-1β, IL-6, TNF-α, TOS, and MDA levels while decreasing GSHPx, GSH, and TAS levels. Increased inflammation and impaired oxidant/antioxidant balance in cardiomyocyte cells after CPL treatment were regulated by LPA treatment. Conclusion: LPA treatment was found to have a protective effect against CPL-induced cardiotoxicity in ... |
Dr. Öğr. Üyesi Yener YAZĞAN
Ramazan Çınar
Dr. Öğr. Üyesi Betül YAZĞAN
