Ginsenoside Rb1 attenuates homocysteine-augmented guidewire injury-induced intimal hyperplasia in mice.
BACKGROUND
Intimal hyperplasia (IH) is the primary cause for post-angioplasty restenosis. The purpose of this study is to investigate the effects of homocysteine (Hcy) and ginsenoside Rb1 (Rb1) on IH using a guidewire injury animal model.


METHODS
In 12-wk-old C57BL/6J mice, the left common carotid artery (CCA) was denudated with a guidewire and the right CCA was used as the uninjured control. They were treated with saline (NS), Hcy, Rb1, or Hcy + Rb1 for 4 wk prior to sacrifice. Animals were sacrificed at 4, 6, or 8 wk. Both CCAs were harvested and intimal-medium thickness (IMT) ratios were calculated. Local macrophage distribution was also studied.


RESULTS
Histology analyses demonstrated consistent internal elastic lamina disruption and focal IH in the injured CCA segments. The degree of IH correlated to the lengths of time following injury. Hcy treated group had significant increase in IMT compared with the NS group (P < 0.05), while Rb1 group was similar to the NS group. In addition, Hcy + Rb1 group showed significant improvement in IMT compared with Hcy group (P < 0.01). Furthermore, Hcy significantly increased local macrophage content as compared with either lesion alone or Rb1 treated animals.


CONCLUSIONS
Our study showed that Hcy increased the degree of IH and macrophage content in the injured CCA and that Rb1 attenuated these adverse effects. These changes might be mediated through antioxidative effects of Rb1. Our data suggests a potential clinical application of ginseng in controlling Hcy-related vascular injuries.
Chai
Hong
H
Division of Vascular and Endovascular Surgery, Department of Surgery, Stanford University, Stanford, California, USA.
Dong
Yanlan
Y
Wang
Xinwen
X
Zhou
Wei
W
D017130:Angioplasty / Q000009:adverse effects* / Q000295:instrumentation; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D020212:Carotid Artery Injuries / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D017536:Carotid Artery, Common / Q000187:drug effects / Q000473:pathology*; D002465:Cell Movement / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D006710:Homocysteine / Q000009:adverse effects* / Q000494:pharmacology; D006965:Hyperplasia / Q000209:etiology / Q000473:pathology / Q000517:prevention & control; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D005894:Panax; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use; D012965:Sodium Chloride / Q000494:pharmacology; D016896:Treatment Outcome; D017539:Tunica Intima / Q000187:drug effects / Q000293:injuries* / Q000473:pathology*
D000975:Antioxidants; D036145:Ginsenosides; D010936:Plant Extracts; D006710:Homocysteine; D012965:Sodium Chloride; C442759:ginsenoside Rb1