CAJ | 학술논문

目的：研究黄芩素( Baicalein, BAI )对核转录因子Nuclear factor erythroid 2-related factor 2(Nrf2)的转录激活,以及对四氯化碳( carbon tetrachloride, CCl4)、乙醇( etha-nol)和对乙酰氨基酚( acetaminophen, APAP)诱导的人正常肝L-02细胞毒性的拮抗作用。方法在肝L-02细胞中,采用瞬时转染报告基因实验检测不同浓度黄芩素对Nrf2转录激活的影响。在 L-02细胞上分别用 APAP (10 mmol · L-1)、CCl4(10 mmol·L-1)、Ethanol (100 mmol·L-1)诱导肝细胞毒性。黄芩素1、10、25、50、100μmol · L-1分别与细胞预孵15 min后,加入上述肝毒性物质,48 h后采用MTT法检测细胞存活率。结果与对照组比较,黄芩素(25、50μmol·L-1)能明显提高 Nrf2的转录激活(P <0．01,P <0．05)。与对照组比较,3种肝毒性物质均能明显降低细胞存活率(P <0．01),而黄芩素能剂量依赖性地提高给予APAP、CCl4和 Ethanol 后降低的 L-02细胞存活率( P <0．01)。结论黄芩素可以诱导重要的抗氧化核转录因子Nrf2的转录激活,这可能是黄芩素拮抗外源性肝毒性物质APAP、CCl4和Ethanol诱导的L-02肝细胞毒性的机制之一。
목적：연구황금소( Baicalein, BAI )대핵전록인자Nuclear factor erythroid 2-related factor 2(Nrf2)적전록격활,이급대사록화탄( carbon tetrachloride, CCl4)、을순( etha-nol)화대을선안기분( acetaminophen, APAP)유도적인정상간L-02세포독성적길항작용。방법재간L-02세포중,채용순시전염보고기인실험검측불동농도황금소대Nrf2전록격활적영향。재 L-02세포상분별용 APAP (10 mmol · L-1)、CCl4(10 mmol·L-1)、Ethanol (100 mmol·L-1)유도간세포독성。황금소1、10、25、50、100μmol · L-1분별여세포예부15 min후,가입상술간독성물질,48 h후채용MTT법검측세포존활솔。결과여대조조비교,황금소(25、50μmol·L-1)능명현제고 Nrf2적전록격활(P <0．01,P <0．05)。여대조조비교,3충간독성물질균능명현강저세포존활솔(P <0．01),이황금소능제량의뢰성지제고급여APAP、CCl4화 Ethanol 후강저적 L-02세포존활솔( P <0．01)。결론황금소가이유도중요적항양화핵전록인자Nrf2적전록격활,저가능시황금소길항외원성간독성물질APAP、CCl4화Ethanol유도적L-02간세포독성적궤제지일。
Aim To study the activation of Nrf2 in-duced by baicalein ( BAI ) , and its protection against carbon tetrachloride ( CCl4 ) , ethanol and acetamino-phen ( APAP )-induced hepatotoxicity. Methods A reporter gene assay was conducted in human normal liver L-02 cells to detect the activation of transcription factor Nrf2 induced by baicalein. APAP ( 10 mmol · L-1 ) , CCl4 (10 mmol·L-1 ) and Ethanol (100 mmol · L-1 ) were used to induce hepatotoxicity in L-02 cells. After the pre-incubation with Baicalein (0, 1, 10, 25, 50, 100 μmol·L-1 ) for 15 min, cells were administrated with or without those above hepatotoxins. 48 h later, cell viability was detected by 3-(4, 5-dim-ethylthiazol-2-yl ) 2 , 5-diphenyltetrazolium bromide (MTT) method. Results Baicalein (25, 50 μmol· L-1 ) induced the activation of Nrf2 ( P <0. 01 , P <0. 05) in the reporter gene assay. As compared with control, three hepatotoxins ( APAP, CCl4 , Ethanol ) all decreased cell viability ( P<0. 01 ) , and baicalein significantly reversed such decreases in a concentra-tion-dependent manner ( P<0. 01 ) . Conclusion Ba-icalein can induce the activation of transcription factor Nrf2 , which is probably one of the mechanisms con-tributing to the protection of baicalein against hepato-toxins (APAP, CCl4, Ethanol)-induced hepatotoxici-ty.