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Chinese Journal of Hepatic Surgery(Electronic Edition) ›› 2014, Vol. 03 ›› Issue (02): 108-111. doi: 10.3877/cma.j.issn.2095-3232.2014.02.011

Special Issue:

• Basic Researches • Previous Articles     Next Articles

Protection and mechanism of naringin on oxidative damage of L02 liver cells

Hui Zhao1, Wei Meng1, Shuhong Yi1,(), Guihua Chen1   

  1. 1. Department of Hepatic Surgery, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, China
  • Received:2014-01-09 Online:2014-04-10 Published:2014-04-10
  • Contact: Shuhong Yi
  • About author:
    Corresponding auther: Yi Shuhong, Email:

Abstract:

Objective

To investigate the protective effect and mechanism of naringin on oxidative damage of L02 liver cells.

Methods

Blank group (L02 liver cells only), naringin group (L02 liver cells with naringin 25 μmol/L), H2O2 damage group (damage group, L02 liver cells with H2O2 200 μmol/L) and protection group (L02 liver cells with H2O2 200 μmol/L and naringin 25 μmol/L) were assigned. Cell viability was evaluated by detecting cell absorbance value (A488). Cell apoptosis rate was detected by flow cytometry. Mitochondrial membrane potential (ΔΨm) was detected by using 5, 5', 6, 6'-tetrachloro-1, 1', 3, 3'-tetrethyl benzimidalyl carbocyanine iodide (JC-1). Malondialdehyde (MDA) was evaluated by detecting cell absorbance value (A532). Reactive oxygen species (ROS) was evaluated by detecting fluorescence intensity by flow cytometry. Superoxide dismutase (SOD) specific activity was detected by using improved xanthine oxidase detection method. Data of these groups were compared by one-way analysis of variance and LSD-t test.

Results

The average cell viability (A488), cell apoptosis rate,ΔΨm were 0.702±0.010, (25.0±0.9)%, 0.95±0.03 respectively in damage group, 0.839±0.032, (14.8±1.7)%, 1.28±0.07 respectively in protection group, and 0.992±0.013, (6.2±0.5)%,1.71±0.08 respectively in blank group. There were significant differences in cell viability, cell apoptosis rate,ΔΨm between damage group and blank group (LSD-t= -27.44, 34.98, -19.88; P<0.05). There were significant differences in cell viability, cell apoptosis rate, Ψm between damage group and protection group (LSD-t=12.94, -18.91, 8.66; P<0.05). The MDA (A532) , ROS (fluorescence intensity) and SOD specific activity were 0.610±0.051, 1 772±69, (67±2)U/g respectively in damage group, 0.346±0.008, 588±24, (111±6)U/g respectively in protective group, 0.121±0.003, 337±17, (159±5)U/g respectively in naringin group, and 0.123±0.007, 375±16, (142±5)U/g respectively in blank group. There were significant differences in ROS and SOD specific activity between naringin group and blank group (LSD-t= -2.24, 5.55; P<0.05). There were significant differences in MDA, ROS and SOD specific activity between damage group and blank group (LSD-t=31.66, 77.85, -24.12; P<0.05). There were significant differences in MDA, ROS and SOD specific activity between protective group and damage group (LSD-t= -17.12, -65.97, 14.03; P<0.05).

Conclusion

Naringin can protect L02 liver cell against oxidative damage by improving its antioxidant capacity.

Key words: Oxidative stress, Naringin, Malondialdehyde, Reperfusion injury, Superoxide dismutase

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