The Ginsenoside Rg1 Prevents Transverse Aortic Constriction–Induced Left Ventricular Hypertrophy and Cardiac Dysfunction by Inhibiting Fibrosis and Enhancing Angiogenesis

Zhang, Yaojun; Zhang, Xin-Lei; Li, Minghui; Iqbal, Javaid; Bourantas, Christos V.; Li, Jingjing; Su, Xiaofei; Muramatsu, Takashi; Tian, Nai‐Liang; Chen, Shao‐Liang

doi:10.1097/fjc.0b013e31828f8d45

Cited by 63 publications

(50 citation statements)

References 31 publications

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“…Ginsenosides exhibit different activities on HIF‐1α and its downstream genes under distinct pathological conditions. For example, HIF‐1α levels were upregulated by Rg1 in neonatal rat brains following hypoxia/ischemia injury and rat heart tissue, as well as by Rb1 in hypoxia neonatal cardiomyocytes . However, HIF‐1α expression is downregulated by Rg3 in several cancer cell lines, including human ovarian cancer cells (e.g., SKOV3 and 3AO, bone marrow stromal cells isolated from acute leukemia patients, and human esophageal carcinoma cells [i.e., EC109, TE1, and KYSE170]) and two tumor mice models, including Lewis lung cancer cell xenografted mice and SKOV3 cells xenografted into nude mice .…”

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

“…For instance, Rg1 plays a neuroprotective role in brain repair after hypoxia/ischemia brain injury through increasing neural survival and facilitating angiogenesis . Rg1 also alleviated the pressure‐overloaded cardiac dysfunction in a rat model of left ventricular hypertrophy induced by transverse aortic constriction, which is at least partly related to enhanced angiogenesis . Rb1 inhibited apoptosis of hypoxia‐insulted neonatal rat cardiomyocytes by upregulating the HIF‐1α‐dependent apelin–APJ system …”

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

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Cellular stress response mechanisms as therapeutic targets of ginsenosides

2017

Medicinal Research Reviews

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Ginseng, one of the most widely used traditional herbal medicines and dietary supplements, has historically been recognized as a tonic herb and adaptogen that can enhance the body's tolerance to various adversities. Ginsenosides are a diverse group of steroidal saponins that comprise the major secondary metabolites of ginseng and are responsible for its multiple pharmacological effects. Emerging evidence suggests that hormetic phytochemicals produced by environmentally stressed plants can activate the moderate cellular stress response mechanisms at a subtoxic level in humans, which may enhance tolerance against severe dysfunction or disease. In this review, we initially describe the role of ginsenosides in the chemical defense of plants from the genus Panax suffering from biotic and abiotic stress. Next, we summarize the diverse evolutionarily conserved cellular stress response pathways regulated by ginsenosides and the subsequent stress tolerance against various dysfunctions or diseases. Finally, the structure-activity relationship involved in the effect of ginsenosides is also analyzed. The evidence presented in this review implicates that ginseng as "the King of all herbs" could be regarded as a well-characterized example of the critical role of cellular stress response mechanisms in understanding the health benefits provided by herbal medicines from an evolutionary and ecological perspective.

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Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

Section: Cellular Stress Response Mechanisms Regulated By Ginsenosidesmentioning

confidence: 99%

Cellular stress response mechanisms as therapeutic targets of ginsenosides

2017

Medicinal Research Reviews

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“…Ginsenoside Rg1 is one of the primary active compounds in P. ginseng and has been shown to inhibit inflammation and oxidative stress [9, 10]. Zhang et al demonstrated that ginsenoside Rg1 could alleviate myocardial fibrosis induced by transverse aortic constriction [11]. Xie et al found that ginsenoside Rg1 significantly attenuated the development of renal interstitial fibrosis in a rat unilateral ureteral obstruction model, perhaps through a reduction of transforming growth factor β 1 (TGF- β 1) [12, 13].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rg1 Ameliorates Cigarette Smoke-Induced Airway Fibrosis by Suppressing the TGF-β1/Smad Pathway In Vivo and In Vitro

Guan

Liu

Han

et al. 2017

BioMed Research International

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Small airway fibrosis is a key pathological process accompanying chronic obstructive pulmonary disease (COPD) and includes fibroblast/myofibroblast transdifferentiation and excessive extracellular matrix deposition. Ginsenoside Rg1, one of the main active ingredients of Panax ginseng, has been shown to exert an antifibrotic effect in many tissues. However, little is known about the underlying mechanism and whether ginsenoside Rg1 can exert an effect on small airway fibrosis. We investigated the anti-small airway fibrosis effects of ginsenoside Rg1 in human embryonic lung fibroblasts and in COPD rats. We found that ginsenoside Rg1 effectively reduced the degree of pulmonary fibrosis, decreased the expression of α-smooth muscle actin, collagen I, and matrix metalloproteinase 9, and maintained the ratio of matrix metalloproteinase 9 to tissue inhibitor of metalloproteinase 1. Importantly, ginsenoside Rg1 significantly attenuated cigarette smoke extract-induced upregulation of transforming growth factor β1, TGF-β receptor I, phospho-Smad2, and phospho-Smad3. In addition, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-β receptor I-Smad2/3 inhibitor. Collectively, these results suggest that ginsenoside Rg1 may suppress cigarette smoke-induced airway fibrosis in pulmonary fibroblasts and COPD rats by inhibiting the TGF-β1/Smad signaling pathway.

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“…26 Moreover, the ginsenosides Rb1 and Rg1, and tetrahydropalmatine enhanced angiogenesis by increasing the expression of hypoxia inducible factor-1 and vascular endothelial growth factor in vivo. [26][27][28] Collectively, bioactive components in Shen-yuan facilitate the recovery of haemodynamic function after MI.…”

Section: Discussionmentioning

confidence: 99%

Effect of Shen-yuan on haemodynamic and anti-inflammatory factors in a porcine model of acute myocardial infarction

et al. 2016

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We previously found that Shen-yuan exerted cardioprotective activities in rodent and porcine myocardial infarction (MI) models because of its antioxidative and anti-apoptotic properties. This study aimed to investigate whether the cardioprotective effects from Shen-yuan are due to regulation of haemodynamics and inflammation in a porcine model of acute MI. Myocardial infarction was induced by left anterior descending coronary artery ligation. Low, moderate, and high doses of Shen-yuan treatment were started 1 week before MI and continued for 2 weeks after MI. Whole blood viscosity at 15 s 21 and platelet aggregation rate were significantly increased in the MI group, but were markedly attenuated by high doses of Shen-yuan. A moderate dose of Shen-yuan also restored decreased values of the peak rise of left ventricular pressure and left ventricular mean pressure after MI. Expression of the T regulatory cell marker forkhead box P3 (Foxp3) + at 14 days post-MI was lower than that in the sham-operated group. Foxp3 was significantly up-regulated in the infarcted and non-infarcted zones of the left ventricle in the Shen-yuan treatment groups. Plasma interleukin-10 and transforming growth factor-b levels were elevated by Shen-yuan treatment in a dose-dependent manner. Shen-yuan elicits cardiovascular protection by its haemodynamic stabilization and anti-inflammatory effects after onset of MI in a porcine model.

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The Ginsenoside Rg1 Prevents Transverse Aortic Constriction–Induced Left Ventricular Hypertrophy and Cardiac Dysfunction by Inhibiting Fibrosis and Enhancing Angiogenesis

Abstract: Ginsenoside Rg1 exhibited protective effect against TAC-induced left ventricular hypertrophy and cardiac dysfunction, which is potentially associated with phospho-Akt activation and p38 MAPK inhibition.

Cited by 63 publications

References 31 publications

Cellular stress response mechanisms as therapeutic targets of ginsenosides

Cellular stress response mechanisms as therapeutic targets of ginsenosides

Ginsenoside Rg1 Ameliorates Cigarette Smoke-Induced Airway Fibrosis by Suppressing the TGF-β1/Smad Pathway In Vivo and In Vitro

Effect of Shen-yuan on haemodynamic and anti-inflammatory factors in a porcine model of acute myocardial infarction

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