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目的:探讨柚皮素(Naringenin)对血管紧张素Ⅱ(AngⅡ)诱导的原代大鼠心肌细胞(NRVMs)肥大作用及其作用机制。方法:AngⅡ刺激NRVMs构建体外心肌肥大模型,分为Vehicle组、Naringenin组、AngⅡ组和AngⅡ+Naringenin组。CCK8检测心肌细胞活性,α-actinin免疫荧光染色检测心肌细胞横截面积,RT-PCR检测ANP、BNP mRNA表达水平,Western Blot检测JNK、ERK及P38蛋白磷酸化水平,Hoechst染色检测心肌细胞凋亡。结果:与对照组相比,AngⅡ组心肌细胞横截面积明显增大,ANP、BNP mRNA表达水平明显增加,给予柚皮素干预后心肌细胞面积减小,ANP、BNP mRNA表达水平降低;此外,柚皮素能够减轻AngⅡ诱导的ERK和P38蛋白磷酸化水平上调及心肌细胞凋亡。结论:柚皮素可以减轻AngⅡ刺激引起的心肌细胞肥大,其机制可能与抑制MAPK信号通路以及减轻心肌细胞凋亡有关。
Objective: To investigate the effects of Naringenin on angiotensin Ⅱ (Ang Ⅱ) -induced primary rat cardiomyocyte (NRVMs) hypertrophy and its mechanism. Methods: Angiotensin Ⅱ (NRⅡ) -induced NRVMs were used to establish a model of cardiac hypertrophy in vitro. The models were divided into Vehicle group, Naringenin group, AngⅡgroup and AngⅡ + Naringenin group. CCK8 was used to measure the activity of cardiomyocytes. The cross-sectional area of cardiomyocytes was detected by α-actinin immunofluorescence staining. The expression of ANP and BNP mRNA was detected by RT-PCR. The phosphorylation of JNK, ERK and P38 was detected by Western Blot. . Results: Compared with the control group, the myocardial cell cross-sectional area was significantly increased and the levels of ANP and BNP mRNA were significantly increased in AngⅡ group. The myocardial cell area was decreased and the expression of ANP and BNP mRNA were decreased after the administration of naringenin. Naringenin can reduce the AngⅡ-induced ERK and P38 protein phosphorylation and cardiac myocyte apoptosis. Conclusion: Naringenin can attenuate cardiomyocyte hypertrophy induced by Ang Ⅱ stimulation. The mechanism may be related to the inhibition of MAPK signaling pathway and the decrease of cardiomyocyte apoptosis.