Chinese Journal of Tissue Engineering Research ›› 2020, Vol. 24 ›› Issue (31): 5052-5056.doi: 10.3969/j.issn.2095-4344.2123

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Protective effects of sulforaphane in a H2O2 induced oxidative stress model of human hepatocytes

Tan Jing1, Yi Guodong2   

  1. 1Department of Nephrorheumatology, 2Department of Gastroenterology, Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, Hubei Province, China
  • Received:2019-01-12 Revised:2019-02-15 Accepted:2019-03-01 Online:2020-11-08 Published:2020-09-04
  • Contact: Yi Guodong, Master, Attending physician, Department of Gastroenterology, Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, Hubei Province, China
  • About author:Tan Jing, Attending physician, Department of Nephrorheumatology, Central Hospital of Enshi Autonomous Prefecture, Enshi 445000, Hubei Province, China

Abstract:

BACKGROUND: Oxidative stress injury plays an important role in the development of chronic hepatitis, and sulforaphane is a natural product with good antioxidant activity.

OBJECTIVE: To investigate the protective effects of sulforaphane on oxidative stress injury of human hepatocytes (LO2) stimulated by H2O2, and to investigate its possible mechanism.

METHODS: LO2 cells were cultured in vitro, followed by 24-hour treatment with 100 μg/L H2O2 to induce the oxidative stress model of the cells. The cells were divided into five groups: control group, model group, sulforaphane treatment groups (low-, middle-, high-dose groups: H2O2+10, 20, and 40 μmol/L sulforaphane, respectively). Cell counting kit-8 was used to measure the relative survival rate of cells, and analyze the levels of oxidative stress products in cell homogenate. Western blot assay was used to determine the expression levels of


nuclear factor erythroid-2 related factor 2 (Nrf2), GCLC, NQO1 and heme oxygenase-1. The study protocol was in accordance with the related ethic requirements of Central Hospital of Enshi Autonomous Prefecture.

RESULTS AND CONCLUSION: H2O2 could induce oxidative stress injury in LO2 cells. Compared with the model group, sulforaphane at various concentrations could significantly induce the proliferation of LO2 cells, inhibit the production of malondialdehyde and nitric oxide, and promote the activity of superoxide dismutase (P < 0.05). Western blot results revealed that sulforaphane could induce the transfer of Nrf2 into the nucleus and significantly increase the expression of GCLC, NQO1, and heme oxygenase-1 proteins (P < 0.05). To conclude, sulforaphane can significantly relieve the oxidative stress injury of LO2 cells induced by H2O2 and its underlying mechanism may be related to the activation of Nrf2 pathway.

Key words: sulforaphane,  human hepatocyte,  oxidative stress,  heme oxygenase-1,  nuclear factor erythroid-2 related factor 2,  protein

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