CAJ | 학술논문

研究了纳米二氧化硅(SiO2)体内及体外氧化应激损伤及细胞毒性作用及机制.体内实验采用ICR小鼠,纳米SiO2经口灌胃染毒3次,检测肺组织中MDA(丙二醛)和SOD(超氧化物歧化酶)含量,观察纳米 SiO2对小鼠肺的氧化应激毒性.采用体外培养的小鼠上皮细胞(JB6细胞),观察不同质量浓度纳米SiO2染毒后的细胞形态改变,通过蛋白免疫印迹实验检测纳米SiO2是否通过FAS 信号途径引起细胞凋亡.研究结果表明:纳米 SiO2经口染毒后对小鼠肺具有氧化应激损伤作用,表现为随染毒剂量的升高,肺组织中 MDA 产生量增加,呈一定的剂量-反应关系.同时,肺组织内 SOD 水平总体趋势降低,但是差别未见统计学意义.体外培养细胞实验中,纳米 SiO2染毒后可引起细胞出现凋亡并呈空泡样变.蛋白免疫印迹实验中,纳米SiO2可引起FAS信号蛋白表达量明显上升,但是FADD表达水平并不升高.
연구료납미이양화규(SiO2)체내급체외양화응격손상급세포독성작용급궤제.체내실험채용ICR소서,납미SiO2경구관위염독3차,검측폐조직중MDA(병이철)화SOD(초양화물기화매)함량,관찰납미 SiO2대소서폐적양화응격독성.채용체외배양적소서상피세포(JB6세포),관찰불동질량농도납미SiO2염독후적세포형태개변,통과단백면역인적실험검측납미SiO2시부통과FAS 신호도경인기세포조망.연구결과표명:납미 SiO2경구염독후대소서폐구유양화응격손상작용,표현위수염독제량적승고,폐조직중 MDA 산생량증가,정일정적제량-반응관계.동시,폐조직내 SOD 수평총체추세강저,단시차별미견통계학의의.체외배양세포실험중,납미 SiO2염독후가인기세포출현조망병정공포양변.단백면역인적실험중,납미SiO2가인기FAS신호단백표체량명현상승,단시FADD표체수평병불승고.
To elucidate the mechanisms of nano-silica induced cytotoxicity and oxidative stress in vivo and in vitro. ICR mice were contaminated using nano-silica three times by oral gavage. The level of MDA (malondialdehyde) and SOD (superoxide dismutase) in the lung tissue were detected as in vivo toxicity endpoints for nano-silica induced oxidative stress. In vitro, mouse epithelial cells (JB6 cells) were cultured, and observed for morphologic changes after treatment with different concentrations of nano-silica. Induction of apoptosis by nano-silica via the FAS signaling pathway was examined by western-blot assay. The result shows that nano-silica induced oxidative stress in mice after oral exposure which is indicated by a significant increase of MDA in lung tissue in a dose-response manner. The SOD levels in lung tissue were decreased. Nano-silica caused oxidative damage in JB6 cells exposed to certain dose ranges. Cell apoptosis were also observed in cells stained with YO-PRO-1 dye. Western blot shows a significant increase in the expression of FAS signaling protein induced by nano-silica. However the level of FADD expression was decreased.