CAJ | 학술논문

目的：分析川芎嗪预处理大鼠肾上腺嗜铬细胞瘤细胞株 PC12细胞后过氧化氢诱导的细胞凋亡情况，探讨川芎嗪抑制脑缺血损伤中氧自由基损伤的分子机制。方法采用川芎嗪预处理 PC12细胞后，制备过氧化氢细胞损伤模型，采用 CCK‐8法活细胞检测、Hoechst‐33342染色、流式细胞术、反转录聚合酶链反应分析细胞凋亡发生机制。结果应用0．0、0．1、1．0、10．0 mmol／L 浓度川芎嗪预处理后，细胞活力分别为（51．2±4．64）％、（58．5±7．46）％、（73．8±2．94）％、（81．0±6．06）％（F＝146．9，P＜0．05），细胞未见大量凋亡小体形成，Bax／Bcl‐2比值降低（F＝2．14，P＜0．05），线粒体膜电位提高，Caspase 3、9活性降低（Caspase 3：F＝1．59，P ＜0．05；Caspase 9：F＝4．98，P＜0．05）。结论川芎嗪预处理后可降低过氧化氢诱导的 PC12细胞凋亡，抑制氧自由基损伤。
목적：분석천궁진예처리대서신상선기락세포류세포주 PC12세포후과양화경유도적세포조망정황，탐토천궁진억제뇌결혈손상중양자유기손상적분자궤제。방법채용천궁진예처리 PC12세포후，제비과양화경세포손상모형，채용 CCK‐8법활세포검측、Hoechst‐33342염색、류식세포술、반전록취합매련반응분석세포조망발생궤제。결과응용0．0、0．1、1．0、10．0 mmol／L 농도천궁진예처리후，세포활력분별위（51．2±4．64）％、（58．5±7．46）％、（73．8±2．94）％、（81．0±6．06）％（F＝146．9，P＜0．05），세포미견대량조망소체형성，Bax／Bcl‐2비치강저（F＝2．14，P＜0．05），선립체막전위제고，Caspase 3、9활성강저（Caspase 3：F＝1．59，P ＜0．05；Caspase 9：F＝4．98，P＜0．05）。결론천궁진예처리후가강저과양화경유도적 PC12세포조망，억제양자유기손상。
Objective To analyze the protection of tetramethylpyrazine to PC12 cells from apoptosis induced by H2 O2 and to explore the inhibition mechanisms of oxygen free radical injury in cerebral ischemia .Methods After the PC12 cells were pretreated by tetramethylpyrazine ,H2 O2 was added to induce the apoptosis of PC12 cells .Vari‐ous methods ,including CCK‐8 live cell test ,Hoechst‐33342 staining ,flow cytometry and quantitative reverse tran‐scription polymerase chain reaction (qRT‐PCR) ,were used to analyze the mechanisms involved in the process . Results After the different concentrations (0 ,0 .1 ,1 ,10 mmol/L ) tetramethylpyrazine pretreatment ,there were no large number of apoptotic bodies formed in PC12 cells and the viability (% )of PC12 cells were (51 .2 ± 4 .64)% , (58 .5 ± 7 .46)% ,(73 .8 ± 2 .94)% and (81 .0 ± 6 .06)% respectively(F= 146 .9 ,P< 0 .05) .Moreover ,in PC12 cells , the rate of Bax /Bcl‐2 dropped(F= 2 .14 ,P< 0 .05) ,the electric potential of mitochondrial membrane enchanced ,ac‐tivity of Caspase 3 and Caspase 9 decreased(Caspase 3 :F= 1 .59 ,P< 0 .05 ;Casapse 9 :F= 4 .98 ,P< 0 .05) .Conclu‐sion The pretreatment with tetramethylpyrazine could reduce the apoptosis of PC12 cells damaged by H2 O2 and in‐hibit oxygen free radical injury .