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

Abstract

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.

Keywords

• Gallik asit
• H9c2 kardiyomiyosit
• kardiyotoksisite
• oksidatif stres
• sisplatin

Ethical Statement

This research was carried out using cells propagated through commercially available cell culture. Ethics committee approval is not required in this study. The study was conducted following the international declaration, guidelines, etc.

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

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.

Keywords

• Cardiotoxicity
• cisplatin
• gallic acid
• H9c2 cardiomyocyte
• oxidative stress

Ethical Statement

This research was carried out using cells propagated through commercially available cell culture. Ethics committee approval is not required in this study. The study was conducted following the international declaration, guidelines, etc.

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