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Published on: June 3, 2018
LPS-enhanced IGF-IIR pathway to induce H9c2 cardiomyoblast cell hypertrophy was attenuated by Carthamus tinctorius
Chum-Liang Tung1,2, Dennis Jine-Yuan Hsieh3,4, Rathinasamy Baskaran5
1Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
Insights
Carthamus tinctorius extract (CTF) prevents heart cell (H9c2) hypertrophy by activating the IGF-1R pathway. This study shows CTF inhibits LPS-induced cardiac hypertrophy, offering potential therapeutic benefits.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Pharmacology
Background:
- Herbal remedies are explored for cardiovascular disease due to lower toxicity.
- The effect of Carthamus tinctorius extract on cardiomyoblast hypertrophy is not well understood.
Purpose of the Study:
- To investigate the protective effects of Carthamus tinctorius extract (CTF) on lipopolysaccharide (LPS)-induced H9c2 cardiomyoblast cell hypertrophy.
- To elucidate the molecular mechanisms underlying CTF's action, focusing on the insulin-like growth factor (IGF) signaling pathway.
Main Methods:
- H9c2 cells were stimulated with LPS and then treated with varying concentrations of CTF.
- Cell size was assessed using actin staining.
- Protein levels of hypertrophic markers (e.g., calcineurin, GATA-4, ANP, BNP) and the IGF-IIR pathway were analyzed via western blot.
- siRNA targeting IGF-IR was used to confirm the role of this receptor.
Main Results:
- CTF significantly reduced LPS-induced H9c2 cell size increase.
- CTF downregulated key hypertrophic proteins including calcineurin, p-GATA-4, GATA-4, atrial natriuretic peptide, and B-type natriuretic peptide.
- CTF inhibited the LPS-induced insulin-like growth factor-II receptor (IGF-IIR) hypertrophy pathway.
- CTF's protective effects were dependent on the activation of IGF-1R, as confirmed by siRNA and inhibitor studies.
Conclusions:
- Carthamus tinctorius extract (CTF) effectively prevents LPS-induced cardiomyoblast hypertrophy in H9c2 cells.
- CTF exerts its protective effect by activating the IGF-1R signaling pathway, which in turn inhibits the IGF-IIR pathway.
- These findings highlight CTF as a potential therapeutic agent for cardiovascular conditions involving cardiac hypertrophy.
Abstract:
The use of herbs as alternative cardiovascular disease treatment has attracted a great deal of attention owing to their lower toxicity. Whether Carthamus tinctorius extract prevent cardiomyoblast cell hypertrophy remains unclear. The present study was performed to investigate the effect of C tinctorius extract (CTF) on rat cardiomyoblast cell H9c2 and the possible molecular mechanisms. H9c2 cells were treated with lipopolysaccharide (LPS; 2 μg/mL) for 12 hours, subsequently treated with CTF (1-25 μg/mL) The incubation continued for another 24 hours, and the cells were analyzed with actin staining assay, western blot analysis, and siRNA transfection assays. In the present study, the increased cell size induced by LPS was significantly decreased by pretreating at a concentration of 1-25 μg/mL CTF. It was found that CTF could inhibit cardiac hypertrophy induced by LPS and decrease hypertrophic proteins calcineurin, p-GATA-4, GATA-4, atrial natriuretic peptide, and B-type natriuretic peptide levels in H9c2 cells. Additionally, LPS-induced insulin-like growth factor-II receptor (IGF-IIR) hypertrophy pathway was downregulated by CTF. Moreover, IGF-IR siRNA or inhibitors both reversed the CTF effects, confirming that CTF activates IGF-1R to prevent LPS-induced H9c2 cardiomyoblast cell hypertrophy. The current findings indicate that CTF activates IGF-IR to inhibit IGF-IIR signaling pathway which resulted in reducing H9c2 cardiomyoblast cell hypertrophy induced by LPS.
