Baicalein protects against cardiac hypertrophy through blocking MEK‐ERK1/2 signaling

Abstract

Baicalein, a flavonoid present in the root of Scutellaria baicalensis, is well known for its antibacterial, antiviral, anti-inflammatory, antithrombotic, and antioxidant effects. Here we show that baicalein also attenuates cardiac hypertrophy. Aortic banding (AB) was performed to induce cardiac hypertrophy secondary to pressure overload in mice. Mouse chow containing 0.05% baicalein (dose: 100 mg/kg/day baicalein) was begun 1 week prior to surgery and continued for 8 weeks after surgery. Our data demonstrated that baicalein prevented cardiac hypertrophy and fibrosis induced by AB, as assessed by echocardiographic and hemodynamic parameters and by pathological and molecular analysis. The inhibitory action of baicalein on cardiac hypertrophy was mediated by effects on mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinases (ERK1/2) signaling and GATA-4 activation. In vitro studies performed in rat cardiac H9c2 cells confirmed that baicalein attenuated cardiomyocyte hypertrophy induced by angiotensin II, which was associated with inhibiting MEK-ERK1/2 signaling. In conclusion, our results suggest that baicalein has protective potential for targeting cardiac hypertrophy and fibrosis through suppression of MEK-ERK1/2 signaling. Baicalein warrants further research as a potential antihypertrophic agent that might be clinically useful to treat cardiac hypertrophy and heart failure.

Baicalein, an active component of Scutellaria baicalensis Georgi, prevents lysophosphatidylcholine-induced cardiac injury by reducing reactive oxygen species production, calcium overload and apoptosis via MAPK pathways

“…Here we show that baicalein attenuated cell death, apoptosis, and [Ca 2+ ]i accumulation of H9c2 cells caused by lysoPC in a dose-dependent manner. Our results are in line with recent investigations showing that baicalein protects against balloon injury-induced intimal hyperplasia and aortic banding-induced cardiac hypertrophy and fibrosis [16,17]. Therefore, baicalein might have the therapeutic utility in the treatment of cardiovascular disease.…”

CB1 cannabinoid receptor antagonist attenuates left ventricular hypertrophy and Akt-mediated cardiac fibrosis in experimental uremia

“…H9c2 rat heart cell is a subclone of the original clonal cell line derived from embryonic BD1X rat heart tissue [53]. Recently, H9c2 is commonly used to investigate the mechanisms underlying the pathophysiology of cardiomyopathy including cardiac fibrosis [54][55][56][57]. In this study, we demonstrated that IS stimulated the CB1R mRNA expression in neonatal mice cardiac fibroblast that is consistent with the expression pattern observed in H9c2 cells.…”

5-, 12- and 15-Hydroxyeicosatetraenoic acids induce cellular hypertrophy in the human ventricular cardiomyocyte, RL-14 cell line, through MAPK- and NF-κB-dependent mechanism

“…The premise of this observation emerges from the fact that the activation of phosphorylated ERK1/2 is crucial for cellular hypertrophy. This is supported by the finding that angiotensin II induced cellular hypertrophy in H9c2 cells through ERK1/2 but not p38 or JNK (Zong et al 2013). Of particular interest in this study, baicalin, LOX inhibitor, blocked the cellular hypertrophy effect of angiotensin II through ERK1/2 signaling pathway (Zong et al 2013).…”