title: Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibiting the expression of peroxiredoxin III in H9c2 cells.
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.
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Mi-Hua
authors.initials: MH
authors.lastname: Liu
authors.affiliation: Department of Pathology, Affiliated Huizhou Hospital of Guangzhou Medical University, The Third People's Hospital of Huizhou, Huizhou, Guangdong 516002, P.R. China.
authors.forename: Xiao-Long
authors.initials: XL
authors.lastname: Lin
authors.affiliation: Department of Cardiology, The First Hospital of Changsha, Changsha, Hunan 410005, P.R. China.
authors.forename: Cong
authors.initials: C
authors.lastname: Yuan
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Jun
authors.initials: J
authors.lastname: He
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Tian-Ping
authors.initials: TP
authors.lastname: Tan
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Shao-Jian
authors.initials: SJ
authors.lastname: Wu
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Shan
authors.initials: S
authors.lastname: Yu
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Li
authors.initials: L
authors.lastname: Chen
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Jun
authors.initials: J
authors.lastname: Liu
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Tian
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Yu-Dan
authors.initials: YD
authors.lastname: Chen
authors.affiliation: Department of Clinical Laboratory, Affiliated Nanhua Hospital, University of South China, Hengyang, Hunan 421001, P.R. China.
authors.forename: Hong-Yun
authors.initials: HY
authors.lastname: Fu
authors.affiliation: Department of Ultrasonic Diagnosis, Bo'ai Hospital of Zhongshan, Zhongshan, Guangdong 528403, P.R. China.
authors.forename: Jian
authors.initials: J
authors.lastname: Li
authors.affiliation: Department of Pathology, Mawangdui Hospital, Changsha, Hunan 410016, P.R. China.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology; D066126:Cardiotoxicity / Q000378:metabolism* / Q000473:pathology; D016923:Cell Death / Q000187:drug effects; D003542:Cystathionine gamma-Lyase / Q000378:metabolism; D019610:Cytoprotection / Q000187:drug effects; D004317:Doxorubicin / Q000633:toxicity*; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D051379:Mice; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D061105:Peroxiredoxin III / Q000378:metabolism*; D013997:Time Factors
chemical_list: D002316:Cardiotonic Agents; D004317:Doxorubicin; D061105:Peroxiredoxin III; D003542:Cystathionine gamma-Lyase; D000111:Acetylcysteine; D006862:Hydrogen Sulfide