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

Sun, Yingying; Liu, Yue; Chen, Ke-ji

doi:10.1007/s11427-016-5007-8

Cited by 77 publications

(46 citation statements)

References 21 publications

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“…The contained ginsenosides may bestow on ginseng various pharmacological actions [ 14 ]. The ginsenosides Rb and Rg1 produce cardioprotective effects [ 15 ]. Ginsenoside Rh2, the active ingredient extracted from red ginseng and with the molecular formula C 36 H 62 O 8 , has been demonstrated to improve ischemic brain injury in rats [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rh2 Improves Cardiac Fibrosis via PPARδ–STAT3 Signaling in Type 1-Like Diabetic Rats

Hsu

Niu

et al. 2017

IJMS

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Ginsenoside Rh2 (Rh2) is an active principal ingredient contained in ginseng (Panax ginseng Meyer), a medicinal herb used to enhance health worldwide. The present study is designed to investigate the effect of Rh2 on myocardial fibrosis in diabetic rats. In a streptozotocin-induced model of type-1 diabetic rats (STZ-diabetic rats), the increased fasting blood glucose levels and heart weight/body weight (HW/BW) ratio were substantially alleviated by Rh2. Moreover, Rh2 improved cardiac performance in STZ-diabetic rats. Histological results from Masson staining showed that Rh2 attenuated cardiac fibrosis in STZ-diabetic rats. The effects of Rh2 were reversed by GSK0660 at a dose sufficient to inhibit peroxisome proliferator-activated receptor δ (PPARδ) in STZ-diabetic rats. The role of PPARδ was subsequently investigated in vitro. Rh2 restored the decreased PPARδ expression level in high glucose-cultured cardiomyocytes. Moreover, increased protein levels of fibrotic signals, including signal transducer and activator of transcription 3 (STAT3), connective tissue growth factor (CCN2) and fibronectin, were reduced by Rh2 in high glucose-cultured cardiomyocytes. These effects of Rh2 were reversed by GSK0660 or siRNA specific for PPARδ Taken together, PPARδ activation may inhibit STAT3 activation to reduce CCN2 and fibronectin expression in diabetic rats with cardiac fibrosis. Moreover, Rh2 improves cardiac function and fibrosis by increasing PPARδ signaling. Therefore, Rh2 is suitable to develop as an alternative remedy for cardiac fibrosis.

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Section: Introductionmentioning

confidence: 99%

Ginsenoside Rh2 Improves Cardiac Fibrosis via PPARδ–STAT3 Signaling in Type 1-Like Diabetic Rats

Hsu

Niu

et al. 2017

IJMS

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“…51 The antiplatelet aggregation activity of ginsenoside Rg 1 and Rb 1 has been reported. 52 In addition, they have activities in treating cardiovascular diseases 53 and ischemic stroke, 54 and have anti-inammatory 55 and neuroprotective effects against cerebral ischemia. 56 Rutin had anti-oxidant, 57 anti-carcinogenic, 58 liver protection, 59 anti-inammatory, 60 neuroprotective, 61 and vasoprotective properties.…”

Section: Discussionmentioning

confidence: 99%

Identification of blood-activating components from Xueshuan Xinmaining Tablet based on the spectrum–effect relationship and network pharmacology analysis

et al. 2020

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“…As an active ingredient of ginseng fruit, GFS plays a crucial role in the treatment of CHD through multiple metabolic pathways including inhibition of platelet aggregation. [171819] The study of Hao et al . [20] showed that Rb1 as an important ingredient of GFS can increase the neural 5-HT concentration and decrease immobility time in the forced swimming test (FST).…”

Section: Introductionmentioning

confidence: 99%

Effects of Ginseng Fruit Saponins on Serotonin System in Sprague-Dawley Rats with Myocardial Infarction, Depression, and Myocardial Infarction Complicated with Depression

Ren

2016

Chinese Medical Journal

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Background:Our previous studies have demonstrated that the levels of 5-hydroxytryptamine (5-HT) and 5-HT 2A receptor (5-HT2AR) in serum and platelet were associated with depression and myocardial infarction (MI), and pretreatment with ginseng fruit saponins (GFS) before MI and depression had an effect on the 5-HT system. In this study, the effects of GFS on the 5-HT system in the Sprague-Dawley (SD) rats with MI, depression, and MI + depression were evaluated.Methods:A total of eighty SD rats were allocated to four groups: MI, depression, MI + depression, and control groups (n = 20 in each group). Each group included two subgroups (n = 10 in each subgroup): Saline treatment subgroup and GFS treatment subgroup. The levels of 5-HT, 5-HT2AR, and serotonin transporter (SERT) were quantified in serum, platelet lysate, and brain tissue through the enzyme-linked immunosorbent assay method, respectively.Results:Compared with those in the saline treatment subgroups, the levels of 5-HT in serum and platelet lysate statistically significantly increased in the GFS treatment subgroups of MI, depression, and MI + depression groups (serum: all P = 0.000; platelet lysate: P = 0.002, 0.000, 0.000, respectively). However, the 5-HT levels in brain homogenate significantly decreased in the GFS treatment subgroups compared with those in the saline treatment subgroups in MI and depression groups (P = 0.025 and 0.044 respectively), and no significant difference was observed between saline and GFS treatment subgroups in MI + depression group (P = 0.663). Compared with that in GFS treatment subgroup of control group, the 5-HT2AR levels in the platelet lysate significantly decreased in GFS treatment subgroups of MI, depression, and MI + depression groups (all P = 0.000). Compared to those in the saline treatment subgroups, the serum SERT levels significantly decreased in the GFS treatment subgroups in MI, depression, and MI + depression groups (P = 0.009, 0.038, and P = 0.001, respectively), while the SERT levels of platelet lysate significantly decreased in GFS treatment subgroup of MI group (P = 0.000), significantly increased in GFS treatment subgroup of depression group (P = 0.019), and slightly changed in GFS treatment subgroup of MI + depression group (P = 0.219). No significant changes for SERT levels in brain homogenate could be found between the saline and GFS treatment subgroups in MI, depression, and MI + depression groups (P = 0.421, 0.076 and P = 0.642).Conclusions:This study indicated that GFS might inhibit the reuptake of 5-HT from serum to platelet according to decreased 5-HT2AR in platelet and SERT in serum and platelet. The change of 5-HT in serum after GFS treatment was inconsistent with that in the brain. It seemed that GFS could not pass through the blood-brain barrier to affect the central serotonergic system.

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

Cited by 77 publications

References 21 publications

Ginsenoside Rh2 Improves Cardiac Fibrosis via PPARδ–STAT3 Signaling in Type 1-Like Diabetic Rats

Ginsenoside Rh2 Improves Cardiac Fibrosis via PPARδ–STAT3 Signaling in Type 1-Like Diabetic Rats

Identification of blood-activating components from Xueshuan Xinmaining Tablet based on the spectrum–effect relationship and network pharmacology analysis

Effects of Ginseng Fruit Saponins on Serotonin System in Sprague-Dawley Rats with Myocardial Infarction, Depression, and Myocardial Infarction Complicated with Depression

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