| 再努热木·艾则孜 热娜古丽·艾则孜 阿得力艾山
阿不力克木 王小英 高冉冉 艾斯卡尔·沙比提△.阿托伐他汀对冠心病大鼠心肌细胞的凋亡及caspase-12表达的影响[J].现代生物医学进展英文版,2015,15(32):6238-6240. |
| 阿托伐他汀对冠心病大鼠心肌细胞的凋亡及caspase-12表达的影响 |
| Atorvastatin on Apoptosis and Caspase-12 Expression in Coronary Artery Disease Rats |
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| DOI： |
| 中文关键词: 阿托伐他汀 冠心病 大鼠 凋亡 caspase-12 |
| 英文关键词: Atorvastatin Coronary artery disease Rat Apoptosis Caspase-12 |
| 基金项目:国家自然科学基金项目（81202773） |
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| 中文摘要: |
| 目的：探讨阿托伐他汀对冠心病大鼠心肌细胞的凋亡及caspase-12 表达的影响。方法：21 只清洁剂SD大鼠经高脂饮食冠心
病造模成功后随机分为空白组、对照组和阿托伐他汀组每组7 只。空白组大鼠未经处理，对照组给予生理盐水10 mL/kg 体重灌
胃，1 天一次连续4 周；阿托伐他汀组大鼠给予阿托伐他汀10 mg/kg 体重灌胃，1 天一次连续4 周。4 周后处死大鼠并取大鼠心肌
组织采用TUNEL法检测细胞凋亡情况，Western-blot法检测caspase-12 表达情况。结果：三组大鼠心肌凋亡比较空白组、对照组
及阿托伐他汀组大鼠细胞凋亡比例分别为(3.72± 0.89) %、(3.84± 1.01) %和(1.47± 0.62) %，阿托伐他汀大鼠心肌细胞凋亡比例明
显低于空白组和对照组（P<0.05）；阿托伐他汀组大鼠心肌细胞Caspase-12 表达水平显著低于空白组与对照组（P<0.05），而空白组
与对照组比较无统计学差异(P>0.05)。结论：阿托伐他汀可能通过抑制大鼠心肌细胞caspase-12 表达来阻断心肌细胞凋亡途径的
激活。 |
| 英文摘要: |
| Objective:To evaluate the effect of atorvastatin on apoptosis and caspase-12 expression in coronary artery disease rats.Methods:21 coronary artery disease rats SD rats were randomly divided into 3 groups (blank group, control group and atorvastatin group)
with each 7 rats in each group. The blank group without any treatment, the control group with 10 mL/kg body weight qd for intragastric
administration for 7 days, and rats in the atorvastatin group were treated with atorvastatin 10 mL/kg body weight qd for intragastric
administration for 7 days. After 7 days the rats were to put to death. The cell apoptosis and caspase-12 expression were arrayed by
TUNEL and Western-blot among the three groups (P>0.05).Results:The apoptosis rate were (3.72± 0.89) %, (3.84± 1.01) % and
(1.47± 0.62) % for the blank, control and atorvastatin groups respectively which indicated that atorvastatin much lower than the blank
and control groups (P<0.05); The caspase-12 expression in atorvastatin group was significant lower than the other two groups with
statistical difference(P<0.05).Conclusion:The cell apoptosis was suppressed by atorvastatin through inhibiting the caspase-12 expression
in coronary artery disease rats. |
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