Hydrogen sulfide attenuates doxorubicin‑induced cardiotoxicity by inhibiting calreticulin expression in H9c2 cells

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

doi:10.3892/mmr.2015.4020

Hydrogen sulfide attenuates doxorubicin‑induced cardiotoxicity by inhibiting calreticulin expression in H9c2 cells

Authors:
- Mi‑Hua Liu
- Yuan Zhang
- Xiao‑Long Lin
- Jun He
- Tian‑Ping Tan
- Shao‑Jian Wu
- Shan Yu
- Li Chen
- Yu‑Dan Chen
- Hong‑Yun Fu
- Cong Yuan
- Jian Li
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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, Mawangdui Hospital, Changsha, Hunan 410016, P.R. China, Department of Pathology, 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, Boai Hospital of Zhongshan, Zhongshan, Guangdong 528403, P.R. China
Published online on: July 2, 2015 https://doi.org/10.3892/mmr.2015.4020
Pages: 5197-5202

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Abstract

Doxorubicin (DOX) is a potent and currently available antitumor therapeutic agent; however, its clinical application is limited by the occurrence of cardiotoxicity. Preliminary evidence indicates that hydrogen sulfide (H2S) may exert protective effects against DOX cardiotoxicity. Therefore, the aim of the present study was to investigate whether calreticulin (CRT) is involved in the cardioprotection of H2S against DOX‑induced cardiotoxicity. DOX was observed to markedly induce injuries, including cytotoxicity and apoptosis, and also enhance the expression level of CRT. Notably, pretreatment of H9c2 cells with sodium hydrosulfide (a donor of H2S) significantly attenuated the decreased cell viability, the increased apoptosis rate and the increased expression level of CRT in H9c2 cells. In addition, pretreatment of H9c2 cells with N‑acetyl‑L‑cysteine, a scavenger of reactive oxygen species (ROS) prior to exposure to DOX, markedly decreased the expression of CRT. These results indicate that exogenous H2S attenuates DOX‑induced cardiotoxicity by inhibiting CRT expression in H9c2 cardiac cells.

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