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Ginsenoside Rb1 prevents homocysteine-induced endothelial dysfunction via PI3K/Akt activation and PKC inhibition
Tao-Hua Lan1, Zhi-Wei Xu, Zhi Wang
1Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, PR China.
Insights
Ginsenoside Rb1 protects against high homocysteine-induced cardiovascular damage by activating PI3K/Akt and inhibiting PKC. This reveals a new mechanism for preventing hyperhomocysteinemia-related heart disease.
Area of Science:
- Cardiovascular Science
- Pharmacology
- Molecular Biology
Background:
- Hyperhomocysteinemia (HHcy) is a risk factor for cardiovascular disease, linked to endothelial dysfunction.
- Ginsenoside Rb1, from ginseng, is known to reduce homocysteine (Hcy)-induced endothelial damage, but its mechanism is unclear.
Purpose of the Study:
- To investigate the protective effects of Ginsenoside Rb1 against Hcy-induced endothelial dysfunction.
- To elucidate the underlying molecular signaling pathways involved in Rb1's action.
Main Methods:
- In vivo and in vitro studies were conducted.
- Endothelium-dependent relaxation and nitric oxide (NO) production were measured.
- Western blotting was used to assess the phosphorylation of endothelial nitric oxide synthase (eNOS) and Akt, and the effects of PI3K/Akt inhibitors and a PKC activator were examined.
Main Results:
- Ginsenoside Rb1 prevented Hcy-induced impairment of endothelium-dependent relaxation and restored NO production.
- Rb1 increased eNOS (serine-1177) and Akt (serine-473) phosphorylation while decreasing eNOS (threonine-495) phosphorylation.
- These effects were mediated via PI3K/Akt activation and protein kinase C (PKC) inhibition.
Conclusions:
- Ginsenoside Rb1 protects against Hcy-induced endothelial dysfunction through the PI3K/Akt pathway activation and PKC inhibition.
- This study reveals a novel mechanism for Ginsenoside Rb1's action.
- Findings suggest potential therapeutic value for Ginsenoside Rb1 in preventing cardiovascular diseases associated with HHcy.
Abstract:
Hyperhomocysteinemia (HHcy), a risk factor for cardiovascular disease, is associated with endothelial dysfunction. Ginsenoside Rb1, the major active constituent of ginseng, potently attenuates homocysteine (Hcy)-induced endothelial damage. However, the underlying mechanism remains unknown. In this study, we have investigated the effect of Ginsenoside Rb1 on Hcy-induced endothelial dysfunction and its underlying signal pathway in vivo and in vitro. Ginsenosides prevented Hcy-induced impairment of endothelium-dependent relaxation and Rb1 reversed Hcy-induced reduction of NO production in a dose-dependent manner as detected by nitrate reductase method. Rb1 activated serine-1177 phosphorylation of endothelial nitric oxide synthase (eNOS) and serine-473 phosphorylation of Akt, while inhibited threonine-495 phosphorylation of eNOS as detected by western blotting. Rb1-induced phosphorylation of serine-1177 was significantly inhibited by wortmannin, PI3K inhibitor or SH-5, an Akt inhibitor, and partially reversed by Phorbol 12-myristate 13-acetate (PMA), a PKC activator. PMA also stimulated phosphorylation of threonine-495 which was inhibited by Rb1. Here we show for the first time that Rb1 prevents Hcy-induced endothelial dysfunction via PI3K/Akt activation and PKC inhibition. These findings demonstrate a novel mechanism of the action of Rb1 that may have value in prevention of HHcy associated cardiovascular disease.
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