Research Papers: Pathology:

Protective effect of hydrogen sulphide against myocardial hypertrophy in mice

Mingjing Shao, Chuanjun Zhuo, Ronghuan Jiang, Guangdong Chen, Jianmin Shan, Jing Ping, Hongjun Tian, Lina Wang, Chongguang Lin and Lirong Hu _

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Oncotarget. 2017; 8:22344-22352. https://doi.org/10.18632/oncotarget.15765

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Mingjing Shao1,*, Chuanjun Zhuo2,3,4,*, Ronghuan Jiang5, Guangdong Chen2, Jianmin Shan2, Jing Ping2, Hongjun Tian3, Lina Wang3, Chongguang Lin2 and Lirong Hu2

1 National Integrated Traditional and Western Medicine Center for Cardiovascular Disease, China-Japan Friendship Hospital, Beijing, China

2 Department of Psychological Medicine, Wenzhou Seventh People’s Hospital, Wenzhou, China

3 Department of Psychological Medicine, Tianjin Anding Hospital, Tianjin, China

4 Department of Psychological Medicine, Tianjin Anning Hospital, Tianjin, China

5 Department of Psychological Medicine, Chinese People’s Liberation Army General Hospital, Chinese People’s Liberation Army Medical School, Beijing, China

* These authors have contributed equally to this work

Correspondence to:

Lirong Hu, email:

Keywords: hydrogen sulfide; cardiac hypertrophy; oxidative stress; Nrf2; Pathology Section

Received: December 12, 2016 Accepted: February 20, 2017 Published: February 27, 2017


Cardiac hypertrophy is a critical component of phenotype in the failing heart. Recently, increasing evidence has demonstrated that oxidative stress plays an important role in the pathogenesis of myocardial hypertrophy. In the present study, we generated a mouse model of transverse aortic constriction (TAC) to investigate whether hydrogen sulfide (H2S) has protective effects against cardiac hypertrophy. Left ventricular structure was analyzed by two-dimensional echocardiography. Oxidative stress was evaluated by measuring malondialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen specie in the myocardium. Angiotensin II (Ang-II) was used to induce cardiomyocyte hypertrophy. Neonatal rat cardiomyocytes pretreated with H2S donor sodium hydrosulfide prior to Ang-II exposure were used to determine the involvement of Nrf2 and PI3K/Akt pathway in the antioxidant effects of H2S. Our findings showed that H2S could protect against cardiac hypertrophy by attenuating oxidative stress. The antioxidant roles of H2S in myocardial hypertrophy probably depend on the activation of PI3K/Akt signaling, which consequently increases Nrf2 activity and HO-1 and GCLM expression. In summary, H2S may exert antioxidant effect on cardiac hypertrophy via PI3K/Akt-dependent activation of Nrf2 pathway.

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