Teaching and Research Section of Traditional Chinese Medicine, Jiangsu Jiankang Vocational College, Nanjing, Jiangsu 210018, P.R. China.
Department of Cardiovascular Medicine, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China.
Mol Med Rep. 2019 Mar;19(3):1551-1560. doi: 10.3892/mmr.2019.9803. Epub 2019 Jan 2.
Luteolin (LTL) serves essential roles in a wide variety of biological processes. Lipopolysaccharide (LPS) can lead to myocardial hypertrophy and autophagy. However, the roles of LTL on LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes have not yet been fully elucidated. In the present study, the morphology of cultured rat cardiomyocytes was observed under an inverted microscope. Cell viability was detected by MTT assay. α‑Actinin and microtubule‑associated protein 1 light chain 3 (LC3) expression levels were measured by immunofluorescence assay. In addition, the expression levels of atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP), LC3, and autophagy‑ and Wnt signaling pathway‑associated genes were analyzed by reverse transcription‑quantitative polymerase chain reaction or western blot assays. The results indicated that LTL increased the cell viability of cardiomyocytes treated with LPS. LTL decreased the expression of cardiac hypertrophy associated markers (ANP and BNP). LTL decreased α‑actinin and LC3 expression levels in LPS‑treated cardiomyocytes. It was also demonstrated that LTL suppressed the mRNA and protein expression levels of LPS‑mediated autophagy and Wnt signaling pathway‑associated genes. In addition, it was demonstrated that silencing of β‑catenin inhibited LPS‑induced cardiomyocyte hypertrophy and the formation of autophagosomes. Thus, the present study suggested that LTL protected against LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes.
木樨草素（LTL）在广泛的生物过程中发挥着重要作用。脂多糖（LPS）可导致心肌肥大和自噬。然而，LTL 在 LPS 诱导的大鼠心肌细胞肥大和自噬中的作用尚未完全阐明。在本研究中，在倒置显微镜下观察培养的大鼠心肌细胞的形态。通过 MTT 检测法检测细胞活力。通过免疫荧光法测定肌球蛋白重链和微管相关蛋白 1 轻链 3（LC3）的表达水平。此外，通过逆转录-定量聚合酶链反应或 Western blot 分析心房利钠肽/脑利钠肽（ANP/BNP）、LC3 和自噬及 Wnt 信号通路相关基因的表达水平。结果表明，LTL 增加了 LPS 处理的心肌细胞的细胞活力。LTL 降低了与心肌肥大相关的标志物（ANP 和 BNP）的表达。LTL 降低了 LPS 处理的心肌细胞中α-肌球蛋白重链和 LC3 的表达水平。此外，研究还表明，LTL 抑制了 LPS 介导的自噬和 Wnt 信号通路相关基因的 mRNA 和蛋白表达水平。此外，沉默β-连环蛋白抑制了 LPS 诱导的心肌细胞肥大和自噬小体的形成。因此，本研究表明 LTL 可防止 LPS 诱导的大鼠心肌细胞肥大和自噬。
