中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
3期
364-366
,共3页
张忠霞%崔冬生%王涛%聂红艳%牛静亚%张睿%周洁%裴运海%李江静%许顺江
張忠霞%崔鼕生%王濤%聶紅豔%牛靜亞%張睿%週潔%裴運海%李江靜%許順江
장충하%최동생%왕도%섭홍염%우정아%장예%주길%배운해%리강정%허순강
乙酰肉碱%缺血预处理%细胞缺氧%葡萄糖%细胞凋亡
乙酰肉堿%缺血預處理%細胞缺氧%葡萄糖%細胞凋亡
을선육감%결혈예처리%세포결양%포도당%세포조망
Acetylcamitine%Ischemic preconditioning%Cell hypoxia%Glucose%Apoptosis
目的 评价乙酰左旋肉碱预处理对低氧低糖诱导PC12细胞凋亡的影响.方法 PC12细胞接种于96孔板中,采用随机数字表法,将细胞随机分为5组(n=6):对照组(C组)、细胞损伤组(Ⅰ组)和不同浓度乙酰左旋肉碱预处理组(A1-3组).C组加入含葡萄糖4.5 g/L的DMEM溶液孵育3h;Ⅰ组加入含葡萄糖0.5 g/L和Na2SO4 3 mmol/L的DMEM溶液孵育3h;A1-3组分别加入0.2、0.4和0.6 mmol/L乙酰左旋肉碱孵育24h,然后加入含葡萄糖0.5 g/L和Na2S2O4 3mmol/L的DMEM溶液孵育3h.采用MTT法检测细胞活力,采用TUNEL法检测细胞凋亡率,测定细胞SOD和ATP酶的活性和MDA含量.结果 与C组比较,Ⅰ组细胞活力降低,细胞凋亡率升高,SOD和ATP酶的活性降低,MDA含量增加(P<0.05),A1-3组细胞活力、细胞凋亡率、SOD和ATP酶的活性和MDA含量差异无统计学意义(P>0.05);与Ⅰ组比较,A1-3组细胞活力升高,细胞凋亡率降低,SOD和ATP酶的活性升高,MDA含量下降(P< 0.05);A1-3组间细胞活力、细胞凋亡率、SOD和ATP酶的活性和MDA含量比较差异无统计学意义(P>0.05).结论 乙酰左旋肉碱预处理可通过抑制细胞凋亡,减轻低氧低糖诱导PC12细胞损伤.
目的 評價乙酰左鏇肉堿預處理對低氧低糖誘導PC12細胞凋亡的影響.方法 PC12細胞接種于96孔闆中,採用隨機數字錶法,將細胞隨機分為5組(n=6):對照組(C組)、細胞損傷組(Ⅰ組)和不同濃度乙酰左鏇肉堿預處理組(A1-3組).C組加入含葡萄糖4.5 g/L的DMEM溶液孵育3h;Ⅰ組加入含葡萄糖0.5 g/L和Na2SO4 3 mmol/L的DMEM溶液孵育3h;A1-3組分彆加入0.2、0.4和0.6 mmol/L乙酰左鏇肉堿孵育24h,然後加入含葡萄糖0.5 g/L和Na2S2O4 3mmol/L的DMEM溶液孵育3h.採用MTT法檢測細胞活力,採用TUNEL法檢測細胞凋亡率,測定細胞SOD和ATP酶的活性和MDA含量.結果 與C組比較,Ⅰ組細胞活力降低,細胞凋亡率升高,SOD和ATP酶的活性降低,MDA含量增加(P<0.05),A1-3組細胞活力、細胞凋亡率、SOD和ATP酶的活性和MDA含量差異無統計學意義(P>0.05);與Ⅰ組比較,A1-3組細胞活力升高,細胞凋亡率降低,SOD和ATP酶的活性升高,MDA含量下降(P< 0.05);A1-3組間細胞活力、細胞凋亡率、SOD和ATP酶的活性和MDA含量比較差異無統計學意義(P>0.05).結論 乙酰左鏇肉堿預處理可通過抑製細胞凋亡,減輕低氧低糖誘導PC12細胞損傷.
목적 평개을선좌선육감예처리대저양저당유도PC12세포조망적영향.방법 PC12세포접충우96공판중,채용수궤수자표법,장세포수궤분위5조(n=6):대조조(C조)、세포손상조(Ⅰ조)화불동농도을선좌선육감예처리조(A1-3조).C조가입함포도당4.5 g/L적DMEM용액부육3h;Ⅰ조가입함포도당0.5 g/L화Na2SO4 3 mmol/L적DMEM용액부육3h;A1-3조분별가입0.2、0.4화0.6 mmol/L을선좌선육감부육24h,연후가입함포도당0.5 g/L화Na2S2O4 3mmol/L적DMEM용액부육3h.채용MTT법검측세포활력,채용TUNEL법검측세포조망솔,측정세포SOD화ATP매적활성화MDA함량.결과 여C조비교,Ⅰ조세포활력강저,세포조망솔승고,SOD화ATP매적활성강저,MDA함량증가(P<0.05),A1-3조세포활력、세포조망솔、SOD화ATP매적활성화MDA함량차이무통계학의의(P>0.05);여Ⅰ조비교,A1-3조세포활력승고,세포조망솔강저,SOD화ATP매적활성승고,MDA함량하강(P< 0.05);A1-3조간세포활력、세포조망솔、SOD화ATP매적활성화MDA함량비교차이무통계학의의(P>0.05).결론 을선좌선육감예처리가통과억제세포조망,감경저양저당유도PC12세포손상.
Objective To investigate the effect of acetyl-L-carnitine (ALC) preconditioning on the PC12 cell apoptosis induced by oxygen-glucose deprivation.Methods PC12 cells were seeded in 96-well plates and randomly divided into 5 groups ( n =6 each):control group (group C),cell injury group (group Ⅰ) and preconditioning with different concentrations of ALC groups (groups A1-3 ).In group C,the cells were incubated with DMEM liquid culture medium containing glucose 0.5 g/L for 3 h.In groups Ⅰ and A1-3 the cells were incubated with DMEM liquid culture medium containing sodium hydrosulfite (Na2S2O4) 3 mmol/L and glucose 0.5 g/L for 3 h,and in addition the cells were pre-incubated with ALC 0.2,0.4 and 0.6 mmol/L for 24 h in groups A1-3 respectively.Cell viability was evaluated by MTF assay,while the apoptosis in cells was detected using TUNEL.The activities of ATPase and SOD and MDA content were also detected.Results Oxygen-glucose deprivation significantly increased the number of apoptotic cells and the content of MDA,and decreased the cell viability and activities of SOD and ATPase in group Ⅰ compared with group C ( P < 0.05).Preconditioning with ALC significantly increased the cell viability and the activities of SOD and ATPaes,and decreased the number of apoptotic cells and the content of MDA in groups A1-3 compared with group Ⅰ ( P < 0.05).Conclusion ALC preconditioning can attenuate PC12 cell injury induced by oxygen-glucose deprivation through inhibition of apoptosis in cells.