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Effect of ligustilide on Ang II-induced hypertrophy in cardiomyocytes and the potential mechanisms.

Lu Q, Luo S, Wen Y - Exp Ther Med (2014)

Bottom Line: The cells were then were stimulated by Ang II and LIG for 1-3 days, following which the cell surface area, intracellular protein concentration, rate of apoptosis and the expression levels of p53, Bcl-2 and Bax were determined.Following stimulation with Ang II, the cell surface area of the neonatal rat myocardial cells increased significantly and the cell morphology was distorted.In addition, administration of LIG restored the expression levels of p53, Bcl-2 and Bax.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemical and Molecular Biology, School of Basic Courses, Guangdong Phamaceutical University, Guangzhou, Guangdong 510006, P.R. China.

ABSTRACT
The aim of the present study was to investigate the effect of ligustilide (LIG) on angiotensin II (Ang II)-induced hypertrophy in neonatal rat myocardial cells and the expression levels of p53, Bcl-2 and Bax. Myocardial cells were isolated and purified from the ventricles of neonate Sprague-Dawley rats (age, 1-3 days) using a differential adhesion method. The cells were then were stimulated by Ang II and LIG for 1-3 days, following which the cell surface area, intracellular protein concentration, rate of apoptosis and the expression levels of p53, Bcl-2 and Bax were determined. Following stimulation with Ang II, the cell surface area of the neonatal rat myocardial cells increased significantly and the cell morphology was distorted. LIG was shown to significantly suppress the Ang II-induced hypertrophy of neonatal rat myocardial cells in a dose-dependent manner. In addition, administration of LIG restored the expression levels of p53, Bcl-2 and Bax. Therefore, LIG can prevent the hypertrophy of cardiomyocytes induced by Ang II, which may be associated with the inhibitory effect that LIG exhibits on cardiomyocyte apoptosis.

No MeSH data available.


Related in: MedlinePlus

Effects of LIG on the hypertrophy of cardiomyocytes (magnification, ×200) in the (A) control at 2 days, (B) control at 3 days, (C) Ang II (1 μg/ml) at 2 days, (D) Ang II (1 μg/ml) at 3 days, (E) Ang II (1 μg/ml) + LIG (100 μg/ml) at 2 days and (F) Ang II (1 μg/ml) + LIG (100 μg/ml) at 3 days. LIG, ligustilide; Ang II, angiotensin II.
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f1-etm-08-01-0169: Effects of LIG on the hypertrophy of cardiomyocytes (magnification, ×200) in the (A) control at 2 days, (B) control at 3 days, (C) Ang II (1 μg/ml) at 2 days, (D) Ang II (1 μg/ml) at 3 days, (E) Ang II (1 μg/ml) + LIG (100 μg/ml) at 2 days and (F) Ang II (1 μg/ml) + LIG (100 μg/ml) at 3 days. LIG, ligustilide; Ang II, angiotensin II.

Mentions: Myocardial cells isolated from neonatal SD rats were cultured normally or treated with Ang II and/or LIG. Control myocardial cells grew adherently and extended their pseudopodia normally. Following two days of culture, the cells became triangular or polygon-shaped and a few single cells even beat spontaneously. Pseudopodia were further interwoven into a network and gradually formed clusters or a monolayer, which appeared radiate in concentric circles. Cells pulsed in synchronicity with complete morphology and good vitality (Fig. 1A and B). However, the cells treated with Ang II exhibited evident distortion and fusion, and the cell surface area increased significantly, indicating that hypertrophy occurred in the primary myocardial cells following treatment with Ang II. Following incubation with Ang II for two or three days, the cells became over-hypertrophic. No clear interval between the cells was observed and the fine pseudopodia were integrated into the intercellular space (Fig. 1C and D). Cells also lost their spontaneous beating ability. However, with regard to the cells treated with 1 μg/ml Ang II and 100 μg/ml LIG for three days, the hypertrophic cells restored their original state of normal myocardial cells (Fig. 1E and F).


Effect of ligustilide on Ang II-induced hypertrophy in cardiomyocytes and the potential mechanisms.

Lu Q, Luo S, Wen Y - Exp Ther Med (2014)

Effects of LIG on the hypertrophy of cardiomyocytes (magnification, ×200) in the (A) control at 2 days, (B) control at 3 days, (C) Ang II (1 μg/ml) at 2 days, (D) Ang II (1 μg/ml) at 3 days, (E) Ang II (1 μg/ml) + LIG (100 μg/ml) at 2 days and (F) Ang II (1 μg/ml) + LIG (100 μg/ml) at 3 days. LIG, ligustilide; Ang II, angiotensin II.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061187&req=5

f1-etm-08-01-0169: Effects of LIG on the hypertrophy of cardiomyocytes (magnification, ×200) in the (A) control at 2 days, (B) control at 3 days, (C) Ang II (1 μg/ml) at 2 days, (D) Ang II (1 μg/ml) at 3 days, (E) Ang II (1 μg/ml) + LIG (100 μg/ml) at 2 days and (F) Ang II (1 μg/ml) + LIG (100 μg/ml) at 3 days. LIG, ligustilide; Ang II, angiotensin II.
Mentions: Myocardial cells isolated from neonatal SD rats were cultured normally or treated with Ang II and/or LIG. Control myocardial cells grew adherently and extended their pseudopodia normally. Following two days of culture, the cells became triangular or polygon-shaped and a few single cells even beat spontaneously. Pseudopodia were further interwoven into a network and gradually formed clusters or a monolayer, which appeared radiate in concentric circles. Cells pulsed in synchronicity with complete morphology and good vitality (Fig. 1A and B). However, the cells treated with Ang II exhibited evident distortion and fusion, and the cell surface area increased significantly, indicating that hypertrophy occurred in the primary myocardial cells following treatment with Ang II. Following incubation with Ang II for two or three days, the cells became over-hypertrophic. No clear interval between the cells was observed and the fine pseudopodia were integrated into the intercellular space (Fig. 1C and D). Cells also lost their spontaneous beating ability. However, with regard to the cells treated with 1 μg/ml Ang II and 100 μg/ml LIG for three days, the hypertrophic cells restored their original state of normal myocardial cells (Fig. 1E and F).

Bottom Line: The cells were then were stimulated by Ang II and LIG for 1-3 days, following which the cell surface area, intracellular protein concentration, rate of apoptosis and the expression levels of p53, Bcl-2 and Bax were determined.Following stimulation with Ang II, the cell surface area of the neonatal rat myocardial cells increased significantly and the cell morphology was distorted.In addition, administration of LIG restored the expression levels of p53, Bcl-2 and Bax.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemical and Molecular Biology, School of Basic Courses, Guangdong Phamaceutical University, Guangzhou, Guangdong 510006, P.R. China.

ABSTRACT
The aim of the present study was to investigate the effect of ligustilide (LIG) on angiotensin II (Ang II)-induced hypertrophy in neonatal rat myocardial cells and the expression levels of p53, Bcl-2 and Bax. Myocardial cells were isolated and purified from the ventricles of neonate Sprague-Dawley rats (age, 1-3 days) using a differential adhesion method. The cells were then were stimulated by Ang II and LIG for 1-3 days, following which the cell surface area, intracellular protein concentration, rate of apoptosis and the expression levels of p53, Bcl-2 and Bax were determined. Following stimulation with Ang II, the cell surface area of the neonatal rat myocardial cells increased significantly and the cell morphology was distorted. LIG was shown to significantly suppress the Ang II-induced hypertrophy of neonatal rat myocardial cells in a dose-dependent manner. In addition, administration of LIG restored the expression levels of p53, Bcl-2 and Bax. Therefore, LIG can prevent the hypertrophy of cardiomyocytes induced by Ang II, which may be associated with the inhibitory effect that LIG exhibits on cardiomyocyte apoptosis.

No MeSH data available.


Related in: MedlinePlus