黄芩茎叶总黄酮对缺氧/复氧诱导心肌细胞凋亡的影响

作者	单位
周晓慧	承德医学院生物化学教研室
杨鹤梅	承德医学院生物化学教研室
刘永平	承德医学院生物化学教研室
龚明玉	承德医学院生物化学教研室

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中文摘要:

目的探讨黄芩茎叶总黄酮(Scuttellaria baicalensissteams-leaf total flavonoids,SSTF)对纯化培养乳鼠心肌细胞缺氧/复氧诱导心肌细胞凋亡的影响及其作用机制。方法选用出生1-2天的SD大鼠60只,雌雄不拘,培养乳鼠心肌细胞,建立缺氧/复氧模型。将培养的心肌细胞分为5组:正常对照组、缺氧/复氧损伤模型组(模型组:缺氧2 h再复氧4 h)、缺氧/复氧损伤加50 mg/L SSTF组(低剂量组)、缺氧/复氧损伤加100 mg/LSSTF组(中剂量组)、缺氧/复氧损伤加200 mg/LSSTF组(高剂量组)。四甲基偶氮唑盐比色法检测细胞存活率,原位末端标记法检测心肌细胞凋亡并计算凋亡率,免疫组织化学法检测心肌细胞Bcl-2、Bax蛋白表达。结果与正常对照组比较,模型组细胞存活率降低,细胞凋亡率升高,Bcl-2蛋白降低,Bax蛋白升高,Bcl-2/Bax蛋白降低,差异均有统计学意义(P<0.01)。与模型组比较,SSTF各剂量组细胞存活率升高,细胞凋亡率降低,Bcl-2蛋白升高,Bax降低,Bcl-2/Bax升高,差异均有统计学意义(P<0.05,P<0.01)。SSTF高剂量组各项指标,与低剂量组比较,差异均有统计学意义(P<0.05)。结论 SSTF对缺氧/复氧诱导的心肌细胞凋亡有保护作用,可能是通过上调Bcl-2蛋白的表达,降低Bax蛋白的表达而发挥作用。

英文摘要:

Objective To study the effect of Scuttellaria baicalensis stem-leaf total flavonoids(SSTF) on cardiocyte apoptosis of neonatal rats induced by hypoxia/reoxygenation and its action of mechanism.Methods Sixty one to two days old rats,male or female,were selected.Hypoxia/reoxygenation injured model was established in cultured cardiocytes of neonate rats.The cultured neonatal rat cardiocytes were divided into 5 groups,i.e.,the normal control group,the hypoxia/reoxygenation injury group(as the model group,cultured cardiocytes were exposed to hypoxia 2 h and subsequently reoxygenated for 4 h),the hypoxia/reoxygenation injury plus 50 mg/L SSTF group(as the low dose SSTF group),the hypoxia/reoxygenation plus 100 mg/L SSTF group(as the middle dose SSTF group),and the hypoxia/reoxygenation plus 200 mg/L SSTF group(as the high dose SSTF group).The cell viability was detected by methylthiazolyl tetrazolium(MTT) colorimetry.The apoptosis of cardiocytes was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL) and the apoptosis rate calculated.The Bcl-2 and Bax protein expressions were determined by immunohistochemistry.Results Compared with the normal control group,the cell viability,Bcl-2 protein contents and Bcl-2/Bax decreased,the apoptosis rate and Bax protein contents increased in the model group(all P<0.01).Compared with the model group,the cell viability,Bcl-2 protein contents and Bcl-2/Bax increased,while the apoptosis rate and Bax protein contents decreased in each SSTF treated group(P<0.05,P<0.01).Compared with the low dose SSTF group,significant difference existed in each index of the high dose SSTF group(all P<0.05).Conclusions SSTF had protection on hypoxia/reoxygenation induced cardiocyte apoptosis.Its protective mechanism might be correlated with its up-regulation of the expression of Bcl-2 protein and down-regulation of the expression of Bax protein.

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