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Journals / Online Türk Sağlık Bilimleri Dergisi / 2024 / Cilt: 9 Sayı: 4

Gallic Acid Attenuates Cisplatin-Induced Apoptosis, Oxidative Stress, and Inflammation in Cardiomyocytes

Gallik Asit Kardiyomiyositlerde Sisplatin ile İndüklenen Apoptoz, Oksidatif Stres ve İnflamasyonu Azaltıyor

Betül Yazğan(KASTAMONU ÜNİ. TIP FAK. FİZYOLOJİ ABD)0000-0002-4029-2007
Yener Yazğan(Faculty of Medicine, Kastamonu University, Kastamonu)0000-0002-5613-6906
Pages
335–341
Publication Date
2024-12-25
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusions: GAL treatment was found to have a protective effect on CIS-induced cardiotoxicity in cardiomyocyte cells.

📌 3 Key Takeaways

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Objective & Hypothesis:Objective: Cisplatin (CIS) is a powerful chemotherapeutic agent that has long been used alone or in combination in the treatment of various cancers.
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Key Findings & Data:Since GAL has broad biological properties and exhibits antioxidant activity, this study aimed to investigate the effect of GAL on CIS-induced cardiotoxicity in H9c2 cardiomyocyte cell lines.
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Conclusion & Impact:Conclusions: GAL treatment was found to have a protective effect on CIS-induced cardiotoxicity in cardiomyocyte cells.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:Gallik asit · H9c2 kardiyomiyosit · kardiyotoksisite

Abstract

Objective: Cisplatin (CIS) is a powerful chemotherapeutic agent that has long been used alone or in combination in the treatment of various cancers. However, the toxicity of CIS in various tissues limits its use. Gallic acid (GAL) has anti-microbial, anti-inflammatory, and anti-tumor properties. Since GAL has broad biological properties and exhibits antioxidant activity, this study aimed to investigate the effect of GAL on CIS-induced cardiotoxicity in H9c2 cardiomyocyte cell lines. Materials and Methods: H9c2 cardiomyocyte cells as control (CON), CIS, and GAL25, GAL50 in combination along with CIS were used. In the analyses made, glutathione (GSH) and glutathione peroxidase (GSH-Px) enzyme activity, lipid peroxidation levels, inflammation markers IL1β, IL 6, and TNF α, Total Oxidant/ Antioxidant (TOS and TAS) status, reactive oxygen species (ROS) and caspase (Casp 3-9) activity in the cells were determined. Results: CIS treatment caused cardiomyocyte cell toxicity and increased Casp 3-9, ROS, IL 1β, TNF α, IL 6, TOS, and MDA levels while decreasing GSH-Px, GSH, and TAS levels. Increased inflammation and impaired oxidant/antioxidant balance in cardiomyocyte cells after CIS treatment were regulated by GAL treatment. Conclusions: GAL treatment was found to have a protective effect on CIS-induced cardiotoxicity in cardiomyocyte cells.

Özet

Amaç: Sisplatin (CIS), çeşitli kanserlerin tedavisinde uzun süredir tek başına veya kombinasyon halinde kullanılan güçlü bir kemoterapötik ajandır. Bununla birlikte, CIS'in çeşitli dokulardaki toksisitesi kullanımını sınırlamaktadır. Gallik asit (GAL) anti-enflamatuar, anti-mikrobiyal ve anti-tümör gibi özelliklere sahiptir. GAL'in geniş biyolojik özelliklere sahip olması ve antioksidan aktivite sergilemesi sebebiyle bu çalışmada GAL'in H9c2 kardiyomiyosit hücre hatlarında CIS kaynaklı kardiyotoksite üzerindeki etkisinin araştırılması amaçlanmıştır. Materyal ve Metot: Kontrol (CON) olarak H9c2 kardiyomiyosit hücreleri, CIS ve CIS ile birlikte GAL25, GAL50 kombinasyonları kullanılmıştır. Çalışmada yapılan analizlerde kardiyomiyosit hücrelerinde Total Antioksidan/Oksidan (TAS ve TOS) durumu, inflamasyon belirteçleri TNF α, IL 1β ve IL 6, lipid peroksidasyon düzeyleri, glutatyon (GSH) ve glutatyon peroksidaz (GSH-Px) enzim aktivitesi, reaktif oksijen türleri (ROS) ve kaspaz aktivitesi (Casp 3-9) belirlenmiştir. Bulgular: Sonuçlar, CIS tedavisinin kardiyomiyosit hücresinde toksisiteye neden olduğunu ve Casp 3-9, ROS, IL 1β, TNF α, IL 6, MDA ve TOS seviyelerini artırırken GSH-Px, GSH ve TAS seviyelerini azalttığını gösterdi. CIS tedavisi sonrasında kardiyomiyosit hücrelerinde artan inflamasyon ve bozulan oksidan/antioksidan dengesi GAL tedavisi ile düzenlenmiştir. Sonuç: GAL tedavisinin kardiyomiyosit hücrelerinde CIS kaynaklı kardiyotoksisite üzerinde koruyucu bir etkiye sahip olduğu bulunmuştur.

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Cite This Article

Yazğan, B., Yazğan, Y. (2024). Gallic Acid Attenuates Cisplatin-Induced Apoptosis, Oxidative Stress, and Inflammation in Cardiomyocytes. Online Türk Sağlık Bilimleri Dergisi, Cilt: 9 Sayı: 4, 335–341. https://doi.org/10.26453/otjhs.1531493

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