Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibiting the expression of peroxiredoxin III in H9c2 cells

Liu,Mi‑Hua; Lin,Xiao‑Long; Yuan,Cong; He,Jun; Tan,Tian‑Ping; Wu,Shao‑Jian; Yu,Shan; Chen,Li; Liu,Jun; Tian,Wei; Chen,Yu‑Dan; Fu,Hong‑Yun; Li,Jian; Zhang,Yuan

doi:10.3892/mmr.2015.4544

Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibiting the expression of peroxiredoxin III in H9c2 cells

Authors:
- Mi‑Hua Liu
- Xiao‑Long Lin
- Cong Yuan
- Jun He
- Tian‑Ping Tan
- Shao‑Jian Wu
- Shan Yu
- Li Chen
- Jun Liu
- Wei Tian
- Yu‑Dan Chen
- Hong‑Yun Fu
- Jian Li
- Yuan Zhang
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Affiliations: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China, Department of Pathology, Affiliated Huizhou Hospital of Guangzhou Medical University, The Third People's Hospital of Huizhou, Huizhou, Guangdong 516002, P.R. China, Department of Cardiology, The First Hospital of Changsha, Changsha, Hunan 410005, P.R. China, Department of Ultrasonic Diagnosis, Bo'ai Hospital of Zhongshan, Zhongshan, Guangdong 528403, P.R. China, Department of Pathology, Mawangdui Hospital, Changsha, Hunan 410016, P.R. China
Published online on: November 11, 2015 https://doi.org/10.3892/mmr.2015.4544
Pages: 367-372

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Abstract

Doxorubicin (DOX) is a widely used chemotherapeutic agent, which can give rise to severe cardiotoxicity, limiting its clinical use. Preliminary evidence suggests that hydrogen sulfide (H2S) may exert protective effects on DOX‑induced cardiotoxicity. Therefore, the aim of the present study was to investigate whether peroxiredoxin III is involved in the cardioprotection of H2S against DOX‑induced cardiotoxicity. The results demonstrated that DOX not only markedly induced injuries, including cytotoxicity and apoptosis, it also increased the expression levels of peroxiredoxin III. Notably, pretreatment with sodium hydrosulfide significantly attenuated the DOX‑induced decrease in cell viability and increase in apoptosis, and also reversed the increased expression levels of peroxiredoxin III in H9c2 cardiomyocytes. In addition, pretreatment of the H9c2 cells with N‑acetyl‑L‑cysteine, a scavenger of reactive oxygen species, prior to exposure to DOX markedly decreased the expression levels of peroxiredoxin III. In conclusion, the results of the present study suggested that exogenous H2S attenuates DOX‑induced cardiotoxicity by inhibiting the expression of peroxiredoxin III in H9c2 cells. In the present study, the apoptosis of H9c2 cardiomyocytes was assessed using an methyl thiazolyl tetrazolium assay and Hoechst staining. The levels of Prx III and cystathionine-γ-lyase were examined by western blotting.

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