Ginsenoside Rb1 inhibits autophagy through regulation of Rho/ROCK and PI3K/mTOR pathways in a pressure-overload heart failure rat model

Yang, Tianrui; Miao, Yun-Bo; Zhang, Tong; Mu, Ninghui; Ruan, Libo; Duan, Jinlan; Zhu, Ying; Zhang, Rongping

doi:10.1111/jphp.12900

Cited by 41 publications

(28 citation statements)

References 23 publications

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“…Ginsenoside Rb1, a saponin extracted from Panax ginseng, could also increase autophagy and reduce apoptosis through inhibiting Rho/ROCK pathway and activating Akt/mTOR pathway. 184 T A B L E 1 Autophagy regulating natural compounds in cardiac diseases Resveratrol and polydatin are both natural monocrystalline compounds extracted from Polygonum cuspidatum.…”

Section: Natural Products In Preventing MImentioning

confidence: 99%

“…Zhang et al 178 demonstrated that berberine attenuates adverse left ventricular remodeling and cardiac dysfunction after acute MI and it enhances autophagy initiation, particularly at a lower dosage in rats. Ginsenoside Rb1, a saponin extracted from Panax ginseng , could also increase autophagy and reduce apoptosis through inhibiting Rho/ROCK pathway and activating Akt/mTOR pathway 184 …”

Section: Natural Products That Modulate Autophagy In Cardiac Diseasesmentioning

confidence: 99%

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Autophagy and cardiac diseases: Therapeutic potential of natural products

Liu

et al. 2020

Medicinal Research Reviews

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The global incidence of cardiac diseases is expected to increase in the coming years, imposing a substantial socioeconomic burden on healthcare systems. Autophagy is a tightly regulated lysosomal degradation mechanism important for cell survival, homeostasis, and function. Accumulating pieces of evidence have indicated a major role of autophagy in the regulation of cardiac homeostasis and function. It is well established that dysregulation of autophagy in cardiomyocytes is involved in cardiac hypertrophy, myocardial infarction, diabetic cardiomyopathy, and heart failure. In this sense, autophagy seems to be an attractive therapeutic target for cardiac diseases. Recently, multiple natural products/phytochemicals, such as resveratrol, berberine, and curcumin have been shown to regulate cardiomyocyte autophagy via different pathways. The autophagy‐modifying capacity of these compounds should be taken into consideration for designing novel therapeutic agents. This review focuses on the role of autophagy in various cardiac diseases and the pharmacological basis and therapeutic potential of reported natural products in cardiac diseases by modifying autophagic processes.

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Section: Natural Products In Preventing MImentioning

confidence: 99%

Section: Natural Products That Modulate Autophagy In Cardiac Diseasesmentioning

confidence: 99%

Autophagy and cardiac diseases: Therapeutic potential of natural products

Liu

et al. 2020

Medicinal Research Reviews

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“…32 It was reported that ginsenoside Rb1 inhibited autophagy through regulation of Rho/ROCK and PI3K/mTOR pathways in a pressure-overload heart failure rat model. 36 On the contrary, ginsenoside Rg1 could promote autophagy and thus inhibit apoptosis via AMPK/mTOR signaling in serum deprivation macrophages. 52,55 Rg1 and Rb1 are 2 major compounds in ginsengs, but the ratios of Rg1/Rb1 are different among the 3 ginsengs.…”

Section: Action On Cardiovascular and Cerebral-vascular Diseasesmentioning

confidence: 99%

“…54 Moreover, PPT-type saponins should be autophagy inhibitors, for example, Rb1. 36,37,39 However, the transformed PPT-type ginsenosides, such as Rg3 58 and Rh2, were autophagy promoters. 73 The PPD-type oligoglycosides were autophagy promoters, for example, Rg1 and its transformed ginsenoside, such as Rh4.…”

Section: Structure-activity Relationship Of Ginsenosides From Notoginseng In Autophagymentioning

confidence: 99%

Sense Ginsenosides From Ginsengs: Structure-Activity Relationship in Autophagy

Kwaku

et al. 2019

Natural Product Communications

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The term ginseng refers to the dried roots of several plants belonging to the genus Panax of the Araliaceae family. The 3 major commercial ginsengs are Panax notoginseng (Burk.) F.H. Chen (Notoginseng), P. ginseng C.A. Meyer (Ginseng), and P. quinquefolius L. (American ginseng), which have been used as herbal medicines. Over 18,000 papers on ginsengs have been published on the basis of their structural diversity and biological activities. Many reviews have summarized the phytochemistry, pharmacology, and clinical use of ginsengs, but the structure-activity relationship (SAR) of ginsenosides from ginsengs in autophagy is unavailable. Herein, we review the structural diversity of ginsenosides, especially the ones in notoginseng, and the SAR in autophagic activity is discussed in detail.

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“…Regarding its effect on AS, previous studies have already shown that the most abundant active component of ginseng, Ginsenoside Rb1 (Rb1), reduces lipid accumulation in macrophage foam cells and enhances atherosclerotic plaque stability [22]. In addition, the close interaction between Rb1 and the PI3K/Akt pathway also supports the anti-atherogenic function of the compound [23]. Therefore, it was reasonable to assess the effect of Rb1 on dysfunctional ECs as well as on the activity of GPER in those cells, which would not only explain the mechanism driving the anti-atherogenic function of Rb1, but also provide a novel treatment agent against EC dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 Prevents Dysfunction of Endothelial Cells by Suppressing Inflammatory Response and Apoptosis in the High-Fat Diet Plus Balloon Catheter-Injured Rabbit Model via the G Protein-Coupled Estrogen Receptor-Mediated Phosphatidylinositol 3-Kinases (PI3K)/Akt Pathway

et al. 2019

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BackgroundThe initiation of atherosclerosis (AS) is attributed to the dysfunction of endothelial cells (ECs) via the inhibition of g protein-coupled estrogen receptor (GPER). In the current study, we assessed the potential of Ginsenoside Rb1 (Rb1) to attenuate the dysfunction of ECs via GPER-mediated PI3K/Akt pathway.Material/MethodsAS was induced in rabbits and then the AS rabbits were treated with Rb1. Thereafter, the ECs were isolated from AS and healthy rabbits, and treated with Rb1. The effect of Rb1 on blood lipid levels in AS rabbits and on apoptosis, inflammatory response, and GPER/PI3K/Akt axis activity in ECs was detected. Furthermore, the activities of GPER and PI3K were modulated to verify the key role of the axis in the anti-AS effect of Rb1.ResultsThe levels of total cholesterol, low-density lipoprotein (LDL), and triglyceride in AS rabbits were suppressed by Rb1 while the high-density lipoprotein (HDL) level was increased. In in vitro assays, Rb1 administration inhibited apoptosis process and the production of pro-inflammation cytokines in AS ECs. The expression levels of GPER, p-PI3K, and p-Akt were upregulated by Rb1, associated with the increased level of Bcl-2 and reduced level of Bax. When the activity of GPER was inhibited by GP-15 in AS ECs, the treatment effect of Rb1 was blocked. However, the activation of PI3K could restore the protective effect of Rb1 after the inhibition of GPER.ConclusionsThe anti-AS potential of Rb1 was exerted by restoring the regular function of ECs via the activation of GPER-mediated PI3K/Akt signaling.

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Ginsenoside Rb1 inhibits autophagy through regulation of Rho/ROCK and PI3K/mTOR pathways in a pressure-overload heart failure rat model

Abstract: The results indicated that Grb1 can exert anti-HF function by inhibiting cardiomyocyte autophagy of rats through regulation of Rho/ROCK and PI3K/mTOR pathways.

Cited by 41 publications

References 23 publications

Autophagy and cardiac diseases: Therapeutic potential of natural products

Autophagy and cardiac diseases: Therapeutic potential of natural products

Sense Ginsenosides From Ginsengs: Structure-Activity Relationship in Autophagy

Ginsenoside Rb1 Prevents Dysfunction of Endothelial Cells by Suppressing Inflammatory Response and Apoptosis in the High-Fat Diet Plus Balloon Catheter-Injured Rabbit Model via the G Protein-Coupled Estrogen Receptor-Mediated Phosphatidylinositol 3-Kinases (PI3K)/Akt Pathway

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