Inhibitory effect of ginsenoside Rb1 on cardiac hypertrophy induced by monocrotaline in rat

Jiang, Qingsong; Huang, Xiao; Dai, Zhi-Kai; Yang, Gui-Zhong; Zhou, Qing; Shi, Jingshan; Wu, Qin

doi:10.1016/j.jep.2007.01.006

Cited by 48 publications

(41 citation statements)

References 21 publications

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“…Rb1 was also shown to inhibit colchicine-induced right ventricular hypertrophy, which may be associated with suppression of calcineurin signaling (Jiang et al, 2007).…”

Section: 1mentioning

confidence: 98%

Roles and mechanisms of ginsenoside in cardiovascular diseases: progress and perspectives

Sun

Liu

Chen

2016

Sci. China Life Sci.

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Ginseng is among the oldest traditional Chinese medicinal herbs and is widely used in China and Southeast Asia. Over the past 50 years, considerable research has focused on the chemical constituents, pharmacological action, and clinical applications of ginseng. In this review, we examine the current state of research on ginseng, including the main active ingredient ginsenoside, its pharmacological effects on the cardiovascular system, and mechanisms of action. We focus on what is known of the effects of ginseng against atherosclerosis, arrhythmia, myocardial ischemia, and its inhibition of ventricular remodeling, providing a basis for expanding the clinical applications of ginseng.

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“…Rb1 was also shown to inhibit colchicine-induced right ventricular hypertrophy, which may be associated with suppression of calcineurin signaling (Jiang et al, 2007).…”

Section: 1mentioning

confidence: 98%

Roles and mechanisms of ginsenoside in cardiovascular diseases: progress and perspectives

Sun

Liu

Chen

2016

Sci. China Life Sci.

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“…Previous studies have demonstrated that ginsenoside Rb1 promotes endothelial nitric oxide production [10], suppresses intimal hyperplasia after vascular injury [11,12,13], protects against endothelial dysfunction [14] and inhibits inflammatory responses in vascular smooth muscle cells [15]. It also suppresses apoptosis and oxidative injury of cardiomyocytes [16,17,18,19,20]; and protect against ischemic-reperfusion injury [21,22], dilated cardiomyopathy [23] and cardiac hypertrophy [24]. A previous study showed that ginsenoside Rb1 can suppress and reverse the development of right heart hypertrophy in monocrotaline (MCT)-treated rats, and the finding was explained by an inhibitory effect of ginsengoside Rb1 on the calcineurin-NFAT signaling pathway in cardiomyocytes [24].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 Attenuates Agonist-Induced Contractile Response via Inhibition of Store-Operated Calcium Entry in Pulmonary Arteries of Normal and Pulmonary Hypertensive Rats

Wang

Jiao

et al. 2015

Cell Physiol Biochem

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Background: Pulmonary hypertension (PH) is characterized by sustained vasoconstriction, enhanced vasoreactivity and vascular remodeling, which leads to right heart failure and death. Despite several treatments are available, many forms of PH are still incurable. Ginsenoside Rb1, a principle active ingredient of Panax ginseng, exhibits multiple pharmacological effects on cardiovascular system, and suppresses monocrotaline (MCT)-induced right heart hypertrophy. However, its effect on the pulmonary vascular functions related to PH is unknown. Methods: We examined the vasorelaxing effects of ginsenoside Rb1 on endothelin-1 (ET-1) induced contraction of pulmonary arteries (PAs) and store-operated Ca²⁺ entry (SOCE) in pulmonary arterial smooth muscle cells (PASMCs) from chronic hypoxia (CH) and MCT-induced PH. Results: Ginsenoside Rb1 elicited concentration-dependent relaxation of ET-1-induced PA contraction. The vasorelaxing effect was unaffected by nifedipine, but abolished by the SOCE blocker Gd³⁺. Ginsenoside Rb1 suppressed cyclopiazonic acid (CPA)-induced PA contraction, and CPA-activated cation entry and Ca²⁺ transient in PASMCs. ET-1 and CPA-induced contraction, and CPA-activated cation entry and Ca²⁺ transients were enhanced in PA and PASMCs of CH and MCT-treated rats; the enhanced responses were abolished by ginsenoside Rb1. Conclusion: Ginsenoside Rb1 attenuates ET-1-induced contractile response via inhibition of SOCE, and it can effectively antagonize the enhanced pulmonary vasoreactivity in PH.

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“…Within more than 30 different ginsenosides, Rb1 has been shown to have beneficial effects on the central nervous system, especially cognitive function like learning and memory (11). Recent studies demonstrated that Rb1 preconditioning has protective effects on myocardial ischemia and reperfusion injury (12) and that Rb1 prevented cardiac myocyte hypertrophy induced by prostaglandin F2 α in vitro (13) and inhibited the right ventricular hypertrophy induced by monocrotaline in vivo (14). However, its potential effect on dilated cardiomyopathy has not been studied either in vivo or in vitro.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside-Rb1 Attenuates Dilated Cardiomyopathy in cTnTR141W Transgenic Mouse

et al. 2010

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Abstract. Familial dilated cardiomyopathy (FDCM) is caused by defective genes and specific medicines are not currently available to treat this. Ginsenoside-Rb1 provides cardioprotection in the experimental models of myocardial ischemia-reperfusion injury. Here we investigate Rb1's effect on DCM in cTnT R141W transgenic mouse. The transgene-positive mice aged 2 months were randomized into the model group and Rb1 [70 mg/(kg·day)] group; transgene-negative mice were used as a control. After 4-month treatment, cardiac function was assessed by echocardiography; cardiac tissues were prepared for histology and electron microscopy. Expression levels of molecular markers of cardiac hypertrophy, fibrosis, and intercalated disc proteins were detected by RT-PCR. Rb1 significantly decreased mortality, chamber dilation, and contractile dysfunction in cTnT R141W mice. Rb1 attenuated cardiac hypertrophy, interstitial fibrosis, ultrastructural degeneration, and intercalated disc remodeling in DCM hearts. Western blotting showed that Rb1 significantly decreased heparin-binding epidermal growth factor-like growth factor (HB-EGF) expression and signal transduction and activators of transcription 3 (STAT3) activation, which were gradually increased in DCM hearts. Our results showed that Rb1 clearly alleviated cardiac dysfunction and remodeling in the cTnT R141W transgenic mouse, indicating its potential utility in the treatment of FDCM.

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Inhibitory effect of ginsenoside Rb1 on cardiac hypertrophy induced by monocrotaline in rat

Cited by 48 publications

References 21 publications

Roles and mechanisms of ginsenoside in cardiovascular diseases: progress and perspectives

Roles and mechanisms of ginsenoside in cardiovascular diseases: progress and perspectives

Ginsenoside Rb1 Attenuates Agonist-Induced Contractile Response via Inhibition of Store-Operated Calcium Entry in Pulmonary Arteries of Normal and Pulmonary Hypertensive Rats

Ginsenoside-Rb1 Attenuates Dilated Cardiomyopathy in cTnTR141W Transgenic Mouse

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