The Inhibitory Effect of Trilinolein on Norepinephrine-Induced β-Myosin Heavy Chain Promoter Activity, Reactive Oxygen Species Generation, and Extracellular Signal-Regulated Kinase Phosphorylation in Neonatal Rat Cardiomyocytes

Abstract

The myocardial protective effects of trilinolein, isolated from the traditional Chinese herb Sanchi (Panax notoginseng), are thought to be related to its antioxidant activity. However, the intracellular mechanism underlying the protective effect of trilinolein in the heart remains unclear. In the present study, we investigated the effect of trilinolein on norepinephrine (NE)-induced protein synthesis in cardiomyocytes. Cultured neonatal rat cardiomyocytes were stimulated with NE, then protein content, [³H]-leucine incorporation, and β-myosin heavy chain (β-MyHC) promoter activity were examined. The effect of trilinolein on NE-induced intracellular reactive oxygen species (ROS) generation was measured with a redox- sensitive fluorescent dye (2′,7′-dichlorofluorescin diacetate) and extracellular signal-regulated kinase (ERK) phosphorylation by Western blotting. Trilinolein inhibited NE-increased protein synthesis, β-MyHC promoter activity, and intracellular ROS. Both trilinolein and the antioxidant, N-acetyl-cysteine, decreased NE- and H₂O₂-induced protein synthesis, β-MyHC promoter activity, and ERK phosphorylation. These data indicate that trilinolein inhibits NE-induced protein synthesis via attenuation of ROS generation in cardiomyocytes.

Protective effect of Korean red ginseng extract on cisplatin ototoxicity in HEI‐OC1 auditory cells

“…The anti-apoptotic effect of Rg1 on neurons can be attributed to enhancing the ratio of Bcl-2 to Bax protein and inhibiting activation of caspase-3 (Chen et al, 2001;. Trilinolein from ginseng extract may be related to anti-ROS activity on myocardial cells (Liu et al, 2004). Ginsenoside from ginseng extract induces neuroprotection in astrocyte cultures through the activation of antioxidant enzymes (Lopez et al, 2007), and ginsenoside Rd may be considered a potential antioxidant against hydrogen peroxide in the PC12 cell line (Ye et al, 2008).…”

Pharmacological activity of sanchi ginseng (Panax notoginseng)

“…Angiotensin IIinduced protein synthesis, -myosin heavy chain promoter activity and production of intracellular reactive oxygen species were inhibited. Angiotensin II-or H 2 O 2 -activated mitogen-activated protein kinase phosphorylation and activator protein-1-(or nuclear factor-kappa B)-reporter activities were reduced (Liu et al 2004a). The aforementioned processes, induced by noradrenaline instead of angiotensin II, were also inhibited by trilinolein .…”

The potential roles of exosomes in pathological cardiomyocyte hypertrophy mechanisms and therapy: A review

“…Hypertrophic stimuli like angiotensin II (Ang II), endothelin-1, catecholamines, cytokines, and biomechanical stretch can increase ROS production in cardiomyocytes. [61,62] This increase in ROS activates hypertrophic signaling mediators and transcription factors such as ERK1/2 and NF-κB, leading to pathological changes. [63] Specifically, ROS produced by NADPH oxidase or mitochondria in pathological cardiac conditions contribute to hypertrophy, fibrosis, reduced contractility, and apoptosis.…”