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KLF15对大鼠心脏压力超/卸负荷后脂质沉积及心功能的调节作用

, PP. 1813-1817

Keywords: 超/卸压力负荷,Kruppel样因子,脂质沉积

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Abstract:

目的通过建立大鼠胸骨上小切口升主动脉缩窄及松解模型,探讨心脏压力超/卸负荷后心脏脂质沉积及心功能的变化。方法选用5周龄、体质量150~200g雄性SD大鼠45只,行非人工通气下胸骨上小切口升主动脉缩窄术致大鼠心脏功能受损,造模成功后分为9组(n=5):假手术对照组(9、12、15周)分别标记为C1、C2、C3,升主动脉缩窄组(缩窄9、12、15周)分别标记为A1、A2、A3,去缩窄组(缩窄9周后去缩窄当天、3、6周组)分别标记为B1、B2、B3。通过动物超声心动图观察心脏功能,PCR和Westernblot检测Kruppel样因子15(kruppel-likefactor15,KLF15),心肌脂质染色观察脂质沉积分别在A1后去缩窄,B1、B2、B3以及A1、A2、A3的变化情况。结果①与C1、C2、C3相比,升主动脉缩窄组随着缩窄时间越长,心功能越低,A1、A2、A3与C1、C2、C3比较EF分别为:[(85.32±3.90)vs(54.32±3.88),(85.45±4.26)vs(47.91±3.64),(82.83±4.93)vs(40.08±4.45),P<0.01];?②与?A1相比,B2、B3心功能有所恢复,并具有统计学差异(P<0.05);EF%:(54.32±3.88)vs(63.28±5.81),(54.32±3.88)vs(63.59±6.48);③与C1、C2、C3相比,A1、B2、B3心脏KLF15mRNA及其蛋白表达降低[mRNA:(0.66±0.09)vs(1.76±0.07),(0.52±0.07)vs(1.78±0.12),(0.51±0.04)vs(1.70±0.13),P<0.01];蛋白:[(0.99±0.05)vs(1.25±0.04),(0.96±0.05)vs(1.30±0.09),(1.01±0.08)vs(1.30±0.06),P<0.01];④与A1相比,B2、B3KLF15mRNA及其蛋白表达无明显变化。⑤与C1、C2、C3相比,A1、B2、B3心脏脂质沉积增多;与A1相比,B2、B3心脏脂质沉积有所减少,但仍明显高于对照组。结论在心脏超/卸负荷中,KLF15可能对心脏脂质沉积具有负向调节作用,参与了卸负荷后心功能的恢复过程。

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