AI Article Synopsis
- Ginsenoside Rg1, derived from Panax notoginseng, may help prevent fibrosis in the heart caused by chronic thromboembolic pulmonary hypertension (CTEPH) according to recent research.
- In an experiment with rats, Rg1 was administered to both normal and CTEPH-affected groups, resulting in reduced heart pressure and improved ratios of right ventricle to left ventricle thickness in those receiving Rg1.
- The study found that Rg1 treatment led to reduced collagen deposition and lower expression of matrix metalloproteinases 2 and 9, suggesting a potential mechanism for its anti-fibrosis effects.
Article Abstract
Background: Recent studies haveshown that ginsenoside Rg1, extracted from the dry roots of Panax notoginseng as a traditional Asian medicine, plays an anti-fibrosis role in myocardial remodeling. However, the mechanism still remains unclear. In the present study, we investigate the effect of ginsenoside Rg1on the collagenic remodeling of myocardium in chronic thromboembolic pulmonary hypertension (CTEPH), and its potential mechanism.
Methods: A rat model of CTEPH was established by injecting thrombi through the jugular vein wice in2 weeks. Four weeks later, four groups (Group A: normal rats + normal saline; Group B: normal rats + Rg1; Group C: CTEPH model + normal saline; Group D: CTEPH model + Rg1) were established. Normal saline and Rg1 were administrated by intraperitoneal injection. Ineach group, we measured the hemodynamic parameters, as well as the right ventricle to left ventricle (RV/LV) thickness ratio. Myocardial tissue sections of the RV were stained by hematoxylin-eosin +gentian violet and the morphological characteristics were observed by light microscopy. The matrix metalloproteinases (MMP) -2 and -9 were detected by the western blot.
Results: Compared with Group A and Group B, the right ventricular systolic pressure was significantly increased in Group C and significantly decreased in Group D. Compared with Group A and Group B, the RV/LV thickness ratio of the rats was significantly higher in Group C and Group D. There was significant fibrosis with collagen in Group C compared with Group A and Group B, and less significant changes in Group D were observed compared with those in Group C. The expression of MMP-2 and MMP-9 exhibited a significant decrease in Group C and was also significantly decreased in Group D compared withGroup A and Group B. Also, a negative linear relationship was shown between collagen-I and the expression of MMP-2 and MMP-9.
Conclusions: Our animal study showed that ginsenoside Rg1 positively affects myocardial remodeling and pulmonary hemodynamics in CTEPH. Upregulation of the expression of MMP-2 and MMP-9 could explain the beneficial effects of ginsenoside Rg1 in CTEPH.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681654 | PMC |
| http://dx.doi.org/10.1186/2047-783X-18-16 | DOI Listing |
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