【摘要】 目的 :通过丹参注射液对培养心肌细胞缺血性损伤中的心肌酶、心肌细胞超微结构和心肌细胞凋亡的影响 ,探讨其保护作用和机制。方法 :将培养第4天的心肌细胞随机分为 4组 :正常对照组 (A组 ) ,缺糖缺氧组 (B组 ) ,小剂量丹参组 (C组 ) ,大剂量丹参组 (D组 ) ,实验结束取培养液上清液检测LDH、α -HBDH ,收集细胞分别做透射电镜及细胞凋亡的检测。结果 :LDH、α -HBDHB组明显高于A组 (P <0 .0 1) ,C组、D组分别低于B组 (P <0 .0 5 ) ,而稍高于A组 (P >0 .0 5 ) ,C组、D组间无统计学意义 (P >0 .0 5 ) ;置显微镜下心肌细胞A组完好 ,B组其内有空泡形成 ,颗粒增加 ,甚至有变性坏死 ,C组、D组细胞也有少量空泡形成 ,细胞核尚正常 ;电镜下心肌细胞A组线粒体结构完好 ,B组可见线粒体肿胀 ,细胞膜不完整。C组、D组仅见少许线粒体肿胀 ,嵴少 ,与A组相近 ;心肌细胞A组有一定的凋亡 ,而B组凋亡数量明显上升 ,与A组相比有统计学意义 (P <0 .0 1) ,C组、D组凋亡数量无统计学意义 (P >0 .0 5 ) ,与B组相比明显下降 (P <0 .0 5 ) ,但仍比A组稍多 (P >0 .0 5 )。结论 :丹参注射液对心肌细胞缺糖缺氧 (缺血性 )损伤有较好的保护作用 ,其机制可能为降低损伤时细胞内酶的漏出 ,减轻心肌细胞缺血性损害超微结构及形态学的变化更多还原

【Abstract】 Objective: Using Dan shen zhusheye (DSZ) to therapy the cultured rat cardiomyocytes which injured under the condition of hypoxia and glucose deprivation and investigating the effect mechanism of DSZ.Methods:Four-days cultured cardiomyocytes were divided into four groups randomly. Group A served as normal control group, while group B as model group (hypoxic and glucose deprivation), group C and D treated with small and large doses DSZ. Then detecting the LDH and α-HBDH. Collecting the cardiomyocytes to detect their apoptosis and to observe their ultramicroscopic structure through transmission electron microscope (TEM).Results:Group B’s level of LDH and α-HBDH is obviously higher than that of group A (P<0.01),group C?D lower than group B (P<0.05) but higher than group A a little (P>0.05) ; No obviously different between C and D (P>0.05). Under the inverted phase contrast microscope.The cardiomyocytes of the group A grow well; under the TEM the mitochondria’s structure was well. In group B, the granular increased, even necrosised, under TEM the mitochondria swellinged, membrance imperfect. While a few mitochondrias swellinged in group C and D.There are some cardiomyocytes apoptosis in group A, while much higher than group A in group B (P<0.01). Comparing with group B, group C and D decrease very much (P<0.05),but increasing a little (P>0.05) comparing with group A, whmore, no obviously different between group C and D.Conclusion:DSZ can better protect cardiomyocyte ischemia injury. The mechanism may be that: 1) Decreasing the cardioenzyme leak; 2)Alleviating the alteration of ultramicroscopic structure; 3) Decreasing the cardiomyocyte apoptosis.更多还原