Chinese Journal of Tissue Engineering Research ›› 2023, Vol. 27 ›› Issue (23): 3621-3627.doi: 10.12307/2023.575

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Serelaxin protects against hypoxia/reoxygenation-induced mouse cardiac microvascular endothelial cell injury by inhibiting oxidative stress responses

Wei Qin1, 2, Chen Bingxin3, Zhao Ling4, Amanguli·Ruze4, Zhao Banghao4, Jiang Tao2, 4, Zhang Chun2, 4, Li Zhiqiang2, 4, Duan Mingjun4, Gao Xiaoming2   

  1. 1Center Laboratory, 4Animal Laboratory Center, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China; 2Xinjiang Key Laboratory of Medical Animal Model Research, Urumqi 830054, Xinjiang Uygur Autonomous Region, China; 3Department of Cardiac Function, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China
  • Received:2022-06-29 Accepted:2022-09-24 Online:2023-08-18 Published:2023-01-14
  • Contact: Duan Mingjun, Master, Assistant researcher, Animal Laboratory Center, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China Gao Xiaoming, MD, Professor, Researcher, Xinjiang Key Laboratory of Medical Animal Model Research, Urumqi 830054, Xinjiang Uygur Autonomous Region, China
  • About author:Wei Qin, Master, Experimentalist, Center Laboratory, Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China; Xinjiang Key Laboratory of Medical Animal Model Research, Urumqi 830054, Xinjiang Uygur Autonomous Region, China Chen Bingxin, Master, Attending physician, Department of Cardiac Function, The First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054, Xinjiang Uygur Autonomous Region, China
  • Supported by:
    Natural Science Foundation of Xinjiang Uygur Autonomous Region, No. 2018D01C197 (to DMJ); the Open Project of the Key Laboratory of Xinjiang Uygur Autonomous Region, No 2021D04020 (to GXM); the Special Project of Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, No. SKL-HIDCA-2021-XXG1 (to ARZ)

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Abstract: BACKGROUND: Serelaxin is a recombinant form of human relaxin 2. As endogenous anti-fibrosis active substances, serelaxin may relieve the symptoms and improve the prognosis of patients with acute heart failure. However, there is no report on the effect of serelaxin on hypoxia/reoxygenation injury of myocardial microvascular endothelial cells (H5V) in mice through regulating oxidative stress.
OBJECTIVE: To investigate the role on serelaxin in a model of hypoxia/reoxygenation-induced mouse cardiac microvascular endothelial cells (H5V)injury.
METHODS: To establish a mouse H5V hypoxia/reoxygenation injury model, cells were incubated under hypoxia for 3, 6, and 12 hours followed by 3 hours of reoxygenation. The optimal time of cellular hypoxia/reoxygenation was determined by cell viability and lactate dehydrogenase activity assay. Different concentrations of serelaxin (0, 60, 100, 140, 180 ng/mL) were selected to act in the H5V cellular hypoxia/reoxygenation injury model, and the optimal drug concentration for drug treatment of cellular hypoxia-reoxygenation injury was determined by the cell viability and lactate dehydrogenase activity assays. H5V cells were then divided into three groups: control, model (hypoxia/reoxygenation), and serelaxin (hypoxia/reoxygenation+180 ng/mL serelaxin) groups. Malondialdehyde, superoxide dismutase and reactive oxygen species levels were detected in each group.
RESULTS AND CONCLUSION: Compared with the control group, cell proliferation was significantly reduced after hypoxia 6 hours/reoxygenation 3 hours and hypoxia 12 hours/reoxygenation 3 hours (P < 0.05), while the lactate dehydrogenase activity in cell supernatant was significantly increased (P < 0.05). Therefore, cells cultured under hypoxia 6 hours/reoxygenation 3 hours were selected for subsequent experiments. Cell viability was significantly increased in the serelaxin group compared with the model group (P < 0.05), while the lactate dehydrogenase activity in cell supernatant was significantly decreased (P < 0.05). Therefore, 180 ng/mL serelaxin was selected for subsequent experiments. Compared with the model group, the serelaxin group showed a significant decrease in reactive oxygen species and malondialdehyde levels but a significant increase in the level of superoxide dismutase (all P < 0.05). To conclude, H5V cells subjected to hypoxia 6 hours/reoxygenation 3 hours could establish a model of H5V vascular endothelial cell injury, and 180ng/mL serelaxin could improve the cell viability and anti-oxidative stress ability. 

Key words: serelaxin, mouse cardiac microvascular endothelial cell, Ischemia-reperfusion injury, malondialdehyde, superoxide dismutase, reactive oxygen species, oxidative stress response

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