探讨柚皮苷（naringin）对L02肝细胞氧化损伤的保护作用及机制。

设立空白组、naringin组、过氧化氢（H₂O₂）损伤组（损伤组）和保护组，其中空白组为L02肝细胞，naringin组为L02肝细胞加入终浓度25 μmol/L的naringin，损伤组为L02肝细胞加入终浓度200 μmol/L的H₂O₂，保护组为L02肝细胞加入终浓度200 μmol/L的H₂O₂和25 μmol/L的naringin。通过检测细胞吸光度值（A₄₈₈）测定细胞活性，流式细胞术检测细胞凋亡率，用四氯四乙基苯并咪唑基羰花青碘化物（JC-1）检测线粒体膜电位（ΔΨm），通过检测细胞吸光度值（A₅₃₂）测定丙二醛（MDA），流式细胞术检测荧光强度测定活性氧自由基（ROS），改良黄嘌呤氧化酶法检测超氧化物歧化酶（SOD）比活力。各组数据比较采用单因素方差分析和LSD-t检验。

损伤组平均细胞活性（A₄₈₈）、细胞凋亡率、ΔΨm分别为0.702±0.010、（25.0±0.9）%、0.95±0.03，保护组相应为0.839±0.032、（14.8±1.7）%、1.28±0.07，空白组相应为0.992±0.013、（6.2±0.5）%、1.71±0.08。损伤组细胞活性、细胞凋亡率、Ψm与空白组比较，差异有统计学意义（LSD-t= -27.44，34.98，-19.88；P<0.05）。保护组细胞活性、细胞凋亡率、Ψm与损伤组比较，差异有统计学意义（LSD-t=12.94，-18.91，8.66；P<0.05）。损伤组MDA （A₅₃₂）、ROS (荧光强度)、SOD分别为0.610±0.051、1 772±69、（67±2）U/g，保护组相应为0.346±0.008、588±24、（111±6）U/g，naringin组相应为0.121±0.003、337±17、（159±5）U/g，空白组相应为0.123±0.007、375±16、（142±5）U/g。naringin组ROS、SOD与空白组比较，差异有统计学意义（LSD-t= -2.24，5.55；P<0.05）。损伤组MDA、ROS、SOD与空白组比较，差异有统计学意义（LSD-t=31.66，77.85，-24.12；P<0.05）。保护组MDA、ROS、SOD与损伤组比较，差异有统计学意义（LSD-t= -17.12，-65.97，14.03；P<0.05）。

naringin通过提高L02肝细胞的抗氧化能力发挥对细胞氧化损伤的保护作用。

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

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.

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).

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