莲房原花青素对乙醇诱导肝细胞DNA损伤的拮抗作用

[目的]研究莲房原花青素(LSPC)对乙醇诱导的人胚肝L-02细胞株DNA损伤的拮抗作用。[方法]观察5、 10、25 mg/L的LSPC与200 mmol/L乙醇共同作用于L-02肝细胞24 h后,对细胞生存率,超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)、丙二醛(MDA)含量,DNA损伤修复酶:[切除修复鼠缺陷交叉互补蛋白1(ERCC1)、O6- 甲基鸟嘌呤甲基转移酶(MGMT)、错配修复hMSH2基因、DNA依赖的蛋白激酶复合物(DNA-PKcs)]表达水平等方面的差异进行比较。[结果]与乙醇组相比,5、10 mg/L的LSPC使细胞的生存率分别由73．14%上升到84．79％和90．52％,细胞SOD、CAT、GSH含量增加(P<0．01),MDA含量减少(P<0．01);有效降低细胞DNA损伤程度(P<0．05)。5 mg/L的 LSPC可显著增加乙醇处理细胞中ERCC1、DNA-PKcs、hMSH2的表达(P<0．01),但对MGMT的表达无影响(P>0．05), 10、25 mg/L的LSPC与乙醇组比较,所有4种DNA损伤修复酶的表达均无明显改变。[结论]适量的LSPC可拮抗乙醇诱导的L-02肝细胞的DNA损伤作用。

Inhibition of Ethanol-induced DNA Damage in Hepatic L-02 Cell Lines by Lotus Seepod Procyanidins

[ Objective ] To study the antagonistic effect of lotus seedpod procyanidins ( LSPC ) on ethanol-induced DNA damage to human embryo liver L-02 cells. [ Methods ] L-02 cells were treated with 200 mmol/L ethanol, 200 mmol/L ethanol 5 mg/L, 10 mg/L or 25 mg/L LSPC respectively for 24 hrs. Survival rate, levels of superoxide dismutase ( SOD ), glutamylcysteinylglycine ( GSH ), catalase ( CAT ), malonyldiadehyde ( MDA ), expression level of DNA damage repair enzymes [ cross-complementing rodent repair deficiency gene1 ( ERCC1 ), O6-methylguanine-DNA methyltransferase ( MGMT ), DNA -dependent protein kinase catalytic subunit ( DNA-PKcs )], hMSH2 were measured. [ Results ] Compared with the ethanol-treated group, the L-02 cell survival rate of 5 and 10 mg/L LSPC groups increased from 73.14% to 84.79% and 90.25%, respectively; SOD, GSH, CAT levels increased ( P < 0.01 ) and MDA level decreased ( P < 0.01 ). But the same effect wasn' t observed in the 25 mg/L LSPC group. In 5 mg/L LSPC group, expression level of ERCC1, DNA-PKcs, hMSH2 increased significantly (P < 0.01 ), but MGMT level was not changed. In 10 mg/L and 25 mg/L LSPC groups, all the 4 DNA damage repair genes had no difference compared with ethanol-treated groups (P > 0.05 ). [ Conclusion ] 5 mg/L LSPC can antagonise ethanol-induced DNA damage in human embryo liver L-02 cells.