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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

Herbal medicines derived from various plant parts have been reported to possess

antioxidant, anti-inflammatory, anti-apoptotic, immunomodulatory, and cardioprotective
properties (Chen et al., 2022). In animals, cardiotoxicity has been linked not only to

phytochemicals present in certain feeds but also to pharmacological and environmental
agents, such as chemotherapeutics, anesthetics, pesticides, and heavy metals, that

adversely affect myocardial cells (Kong et al., 2022; Yurdakok-Dikmen & Filazi, 2025).

NF-κB is a ubiquitous transcription factor that plays a pivotal role in regulating
inflammation. Upon activation, NF-κB induces the expression of multiple pro-inflammatory
cytokines, including TNF-α, IL-1β, and IL-6, contributing to myocardial inflammation,

ischemia/reperfusion injury, hypertrophy, and apoptosis (Gu et al., 2024). Exposure to

cardiotoxic agents, such as lipopolysaccharide, doxorubicin, and cisplatin, activates NF-κB
signaling in cardiac cells, leading to the upregulation of TNF-α and other inflammatory

mediators, which subsequently promote cellular injury and cardiac dysfunction (Shi et al.,
2023; Xia et al., 2022; Zhang & Zhang, 2018).

Substantial evidence indicates that NF-κB is critically involved in the release of
inflammatory mediators during DOX-induced inflammation in myoblasts. Elevated TNF-α

levels promote apoptosis and inflammation in cardiomyocytes, and sustained elevation is

associated with myocardial damage, heart failure, and ventricular dysfunction (Bergmann et
al., 2001; Guo et al., 2013). In this study, we demonstrated that exposure to doxorubicin

significantly increased NF-κB mRNA expression in H9c2 cells, which subsequently led to a
marked upregulation of TNF-α expression. Several studies have demonstrated that

doxorubicin-induced H9c2 cells exhibit increased levels of proinflammatory cytokines such
as TNF-α, IL-1β, and IL-6. Consistent with prior research, our results indicated that treatment

with 5 µM resulted in an upregulation of NF-κB and TNF-α mRNA expression, thereby
confirming the successful establishment of a cardiotoxicity model in H9c2 cells.

Pretreatment with 20 and 40 µg/ml BSO effectively diminished doxorubicin-induced NF-κB
expression, thereby reducing TNF-α expression. Significantly, 40 µg/ml BSO effectively

suppressed NF-κB expression to levels similar to those observed in the control group. This

indicated that the anti-inflammatory properties of BSO are closely linked to the suppression
of NF-κB signaling.

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