参芪益心方抑制阿霉素诱导心肌细胞凋亡作用研究
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摘要
目的:证实参芪益心方可以抑制阿霉素诱导的心肌细胞凋亡。方法:用SD大鼠制备含药血清,用阿霉素诱导H9c2心肌细胞凋亡建立模型,将细胞设置为空白对照组、模型组、含药血清高剂量组(8%)、含药血清中剂量组(4%)、含药血清低剂量组(2%)和卡托普利组。含药血清提前预处理,阿霉素造模72 h后进行试验检测,倒置显微镜下观察H9c2心肌细胞形态,MTT法检测细胞增殖活性;Annexin V-FITC/PI双染法检测H9c2心肌细胞凋亡。结果:H9c2心肌细胞形态:参芪益心方含药血清高、中、低剂量组及卡托普利组可改善细胞凋亡现象,其中以含药血清高剂量组、卡托普利组改善最为明显。MTT法检测H9c2心肌细胞增殖率:模型组OD值、增殖率与空白对照组比较差异具有统计学意义(P<0.01);含药血清高、中、低剂量组及卡托普利组OD值、增殖率与模型组比较差异具有统计学意义(P<0.05,P<0.01);含药血清高剂量组与卡托普利组OD值比较,差异无统计学意义(P>0.05)。流式细胞仪测得结果示:与空白对照组比较,模型组细胞凋亡数量(Q2+Q4)明显增多;含药血清预处理后(Q2+Q4)明显降低,含药血清高、中剂量组及卡托普利组与模型组比较差异具有统计学意义(P<0.01)。结论:参芪益心方可以抑制阿霉素诱导的细胞凋亡。
Objective :To prove that Shenqi Yixin Decoction can inhibit apoptosis of myocardial cells induced by doxorubicin. Methods :Drug serum was prepared from SD rats. The apoptosis of H9 c2 myocardial cells was induced by adriamycin. The cells were set as blank control group,model group,high dose group(8%),medium dose group(4%),low dose group(2%)and captopril group. Drug serum was pretreated and doxorubicin was moulded for 72 h. The morphology of H9 c2 myocardial cells was observed under inverted microscope,and the proliferation activity was detected by MTT. Annexin V-FITC/PI double staining test H9 c2 cardiomyocytes apoptosis. Results :The morphology of H9 c2 myocardial cells :the apoptosis was improved in the high,medium,low dose and captopril groups,especially in the high dose and captopril groups. MTT method was used to detect the productivity rate of H9 c2 myocardial cells :the difference of the OD value and the value-added rate between the model group and the blank group was statistically significant(P<0.01). Compared with the model group,the OD value and the value-added rate of the high,medium and low drug serum groups,captopril group were statistically significant(P<0.05,P<0.01). There was no statistically significant difference(P>0.05)in OD value between the high-dose drug serum group and the captopril group. The results obtained by flow cytometry showed that the number of apoptosis(Q2+Q4)was significantly increased in the model group compared with the blank control group. After the pretreatment of serum containing drugs(Q2+Q4),it was significantly reduced,and the comparison between high dose group,medium dose group and captopril group and the model group was statistically significant(P<0.01). Conclusion :Shenqi YixinDecoction can inhibit apoptosis induced by doxorubicin.
Objective :To prove that Shenqi Yixin Decoction can inhibit apoptosis of myocardial cells induced by doxorubicin. Methods :Drug serum was prepared from SD rats. The apoptosis of H9 c2 myocardial cells was induced by adriamycin. The cells were set as blank control group,model group,high dose group(8%),medium dose group(4%),low dose group(2%)and captopril group. Drug serum was pretreated and doxorubicin was moulded for 72 h. The morphology of H9 c2 myocardial cells was observed under inverted microscope,and the proliferation activity was detected by MTT. Annexin V-FITC/PI double staining test H9 c2 cardiomyocytes apoptosis. Results :The morphology of H9 c2 myocardial cells :the apoptosis was improved in the high,medium,low dose and captopril groups,especially in the high dose and captopril groups. MTT method was used to detect the productivity rate of H9 c2 myocardial cells :the difference of the OD value and the value-added rate between the model group and the blank group was statistically significant(P<0.01). Compared with the model group,the OD value and the value-added rate of the high,medium and low drug serum groups,captopril group were statistically significant(P<0.05,P<0.01). There was no statistically significant difference(P>0.05)in OD value between the high-dose drug serum group and the captopril group. The results obtained by flow cytometry showed that the number of apoptosis(Q2+Q4)was significantly increased in the model group compared with the blank control group. After the pretreatment of serum containing drugs(Q2+Q4),it was significantly reduced,and the comparison between high dose group,medium dose group and captopril group and the model group was statistically significant(P<0.01). Conclusion :Shenqi YixinDecoction can inhibit apoptosis induced by doxorubicin.
引文
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[16]樊理华,韩新.阿霉素对大鼠原代心肌细胞凋亡的影响[J].中华全科医学,2013,11(8):1167-1168.
[17]郭茜茜,于广,吴丹丹,等.阿霉素对大鼠原代心肌细胞调亡的影响[J].免疫学杂志,2015,31(5):425-426.
[2]金娟,吴丹,邹国良,等.参芪益心方对CHF大鼠心肌细胞凋亡指数及Bax、Bcl-2表达的影响[J].山东中医杂志,2014,33(5):388-390.
[3]刘莉,王智怡,姚春丽,等.益气温阳、活血利水法治疗慢性心力衰竭的研究进展[J].中医临床研究,2018,10(20):138-141.
[4]黄小玲,唐轶洋,钟敏,等.不同缺氧复氧损伤程度对H9c2心肌细胞自噬的影响[J].实用医学杂志,2018,34(13):2165-2168.
[5]孙政华,邵晶,郭玫.黄芪化学成分及药理作用研究进展[J].中医临床研究,2015,25(7):22-25.
[6]闫海峰,代向东,樊克涛,等.人参皂苷Re对ADP、PAF、AA诱导家兔血小板聚集功能的影响[J].天津中医药大学学报,2016,35(5):310-313.
[7]王巍,苏光悦,胡婉琦,等.近10年人参皂苷对心血管疾病的药理作用研究进展[J].中草药,2016,47(20):3736-3741.
[8]李淑清.丹参川芎嗪注射液联合单硝酸异山梨酯注射液治疗冠心病心绞痛的疗效研究[J].中国医学创新,2018(26):28-32.
[9]梁志培.茯苓化学成分、药理作用及临床应用研究进展[J].中国城乡企业卫生,2018,33(8):51-53.
[10]胡彦武,刘凯,闫梦彤,等.淫羊藿总黄酮及淫羊藿苷的心血管保护作用及机制研究进展[J].中国实验方剂学杂志,2015,21(13):227-230.
[11]靳淼,刘思余.仙鹤草研究进展[J].安徽农业科学,2015,43(19):78-79,115.
[12]张国顺,白义萍,王小兰,等.葶苈子抗心衰有效组分筛选及其作用机制分析[J].中国实验方剂学杂志,2017,23(4):118-125.
[13]郭娟,陈长勋.葶苈子水提液对动物实验性心室重构的影响[J].中草药,2007,38(10):1519-1560.
[14]邓青秀,彭成.中医药心力衰竭动物模型的研究现状[J].四川动物,2011,30(2):68-69.
[15]张媛.AMPK活化在HaS括抗阿霉素诱导大鼠H9c2也肌细胞凋亡中的作用[D].衡阳:南华大学,2014.
[16]樊理华,韩新.阿霉素对大鼠原代心肌细胞凋亡的影响[J].中华全科医学,2013,11(8):1167-1168.
[17]郭茜茜,于广,吴丹丹,等.阿霉素对大鼠原代心肌细胞调亡的影响[J].免疫学杂志,2015,31(5):425-426.