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HEART FAILURE / EXPERIMENTAL RESEARCH
Emodin improves the cardiac function in the rats with chronic heart failure through regulation of the miR-26b-5p/PTEN pathway
1
Department of Cardiovasology, The Second People’s Hospital of Lianyungang, Jiangsu, China
Submission date: 2019-08-13
Final revision date: 2019-10-14
Acceptance date: 2019-11-19
Online publication date: 2020-06-15
Publication date: 2024-04-23
Arch Med Sci 2024;20(2):655-663
KEYWORDS
TOPICS
ABSTRACT
Introduction:
Chronic heart failure (CHF) is a leading cause of deaths induced by cardiovascular disease. This study aimed to investigate the protective effects of emodin in CHF rats and explore the related mechanisms.
Material and methods:
A total of 56 Wistar rats were used to construct CHF model using the coronary artery ligation. The effects of emodin on cardiac function and inflammation were analyzed in the CHF rats. Expression of miR-26b-5p in the CHF model before and after emodin treatment was estimated by quantitative real-time polymerase chain reaction. The effects of miR-26b-5p on cardiac function and inflammation were also assessed, and its target gene was predicted and confirmed in rat cardiomyocyte H9c2.
Results:
Emodin treatment could significant improve the cardiac function and inflammation evidenced by the increased increased ejection fraction (EF), fractional shortening (FS), left ventricular systolic pressure (LVSP) and maximum of the first differentiation of left ventricular pressure (+LV dP/dtmax) and decreased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), left ventricular end diastolic pressure (LVEDP), interleukin (IL)-6, tumor necrosis factor α (TNF-α) levels. Expression of miR-26b-5p was downregulated in the CHF rats (CHF 0.442 ±0.131 vs. Sham 1.044 ±0.160), and this suppressive effect was rescued by emodin (Emodin 0.902 ±0.132 vs. CHF 0.442 ±0.131). The overexpression of miR-26b-5p in CHF rats led to improved cardiac function and inflammatory response. In addition, the emodin-induced increased EF, FS, LVSP and +LV dP/dtmax and decreased ANP, BNP, LVEDP, IL-6 and TNF-α were all abrogated by the knockdown of miR-26b-5p. The target prediction results revealed that PTEN was a target gene of miR-26b-5p in H9c2 cells.
Conclusions:
All the results indicated that emodin serves a protective role in CHF via regulation of the miR-26b-5p/PTEN pathway. Emodin may be an effective therapeutic agent for CHF treatment.
Chronic heart failure (CHF) is a leading cause of deaths induced by cardiovascular disease. This study aimed to investigate the protective effects of emodin in CHF rats and explore the related mechanisms.
Material and methods:
A total of 56 Wistar rats were used to construct CHF model using the coronary artery ligation. The effects of emodin on cardiac function and inflammation were analyzed in the CHF rats. Expression of miR-26b-5p in the CHF model before and after emodin treatment was estimated by quantitative real-time polymerase chain reaction. The effects of miR-26b-5p on cardiac function and inflammation were also assessed, and its target gene was predicted and confirmed in rat cardiomyocyte H9c2.
Results:
Emodin treatment could significant improve the cardiac function and inflammation evidenced by the increased increased ejection fraction (EF), fractional shortening (FS), left ventricular systolic pressure (LVSP) and maximum of the first differentiation of left ventricular pressure (+LV dP/dtmax) and decreased atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), left ventricular end diastolic pressure (LVEDP), interleukin (IL)-6, tumor necrosis factor α (TNF-α) levels. Expression of miR-26b-5p was downregulated in the CHF rats (CHF 0.442 ±0.131 vs. Sham 1.044 ±0.160), and this suppressive effect was rescued by emodin (Emodin 0.902 ±0.132 vs. CHF 0.442 ±0.131). The overexpression of miR-26b-5p in CHF rats led to improved cardiac function and inflammatory response. In addition, the emodin-induced increased EF, FS, LVSP and +LV dP/dtmax and decreased ANP, BNP, LVEDP, IL-6 and TNF-α were all abrogated by the knockdown of miR-26b-5p. The target prediction results revealed that PTEN was a target gene of miR-26b-5p in H9c2 cells.
Conclusions:
All the results indicated that emodin serves a protective role in CHF via regulation of the miR-26b-5p/PTEN pathway. Emodin may be an effective therapeutic agent for CHF treatment.
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