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目的:探讨黄芪甲苷(astragalosideⅣ,As-Ⅳ)对血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)诱导的乳鼠心肌细胞肥大的作用及机制。方法:以原代培养乳鼠心肌细胞为模型,血管紧张素Ⅱ0.1μmol/L诱导心肌细胞肥大。观察黄芪甲苷3μmol/L、10μmol/L、30μmol/L浓度对心肌肥厚的抑制作用,并进一步探索在钙调素激酶Ⅱ(CaMKⅡ)特异性抑制剂KN93及血管紧张素Ⅱ拮抗剂Losartan存在的情况下,对心肌肥厚的作用。用Lowry法测心肌细胞蛋白含量;消化分离法及计算机图像分析系统测细胞体积;以Fura-2/AM为荧光探针,采用Till阳离子测定系统,观察胞内[Ca2+]i瞬间变化;Western blot法测心肌细胞内CaMKⅡδB表达。结果:与正常组比,血管紧张素Ⅱ0.1μmol/L组心肌细胞总蛋白含量增加了61.4%,体积增大了88.6%,心肌细胞内[Ca2+]i静息水平提高,CaMKⅡδB的表达明显增加;洛沙坦1μmol/L及钙调素激酶Ⅱ特异性抑制剂0.2μmol/L明显抑制了血管紧张素Ⅱ诱导的上述改变。结论:黄芪甲苷对血管紧张素Ⅱ诱导的乳鼠心肌细胞肥大有抑制作用,其机制可能与降低[Ca2+]i及CaMKⅡδB表达有关。
Objective: To investigate the effect and mechanism of astragaloside Ⅳ (As-Ⅳ) on the hypertrophy of neonatal rat cardiomyocytes induced by angiotensinⅡ (AngⅡ). Methods: Primary cultured neonatal rat cardiomyocytes were used as model. Angiotensin Ⅱ 0.1 μmol / L induced cardiomyocyte hypertrophy. To observe the inhibitory effect of astragaloside 3μmol / L, 10μmol / L and 30μmol / L on myocardial hypertrophy, and to further explore the existence of calcineurin Ⅱ (CaMKⅡ) specific inhibitor KN93 and angiotensin Ⅱ antagonist Losartan Case, the role of myocardial hypertrophy. The protein content of cardiomyocytes was measured by Lowry method. The cell volume was measured by digestion and computerized image analysis system. The transient intracellular Ca2 + i change was observed by Fura-2 / AM fluorescent probe using the Till cation assay system. Western blot Method to measure the expression of CaMKⅡδB in cardiomyocytes. Results Compared with the normal group, the total protein content of cardiomyocytes increased by 61.4% and the volume increased by 88.6% in angiotensin Ⅱ 0.1μmol / L group, while the resting level of [Ca2 +] i in myocardial cells increased and the expression of CaMKⅡδB increased ; Losartan 1μmol / L and calmodulin kinase Ⅱ specific inhibitor 0.2μmol / L significantly inhibited the above changes induced by angiotensin Ⅱ. CONCLUSION: Astragaloside inhibits the hypertrophy of neonatal rat cardiomyocytes induced by angiotensin Ⅱ, and its mechanism may be related to the decrease of [Ca2 +] i and the expression of CaMKⅡδB.