||Protopanaxdiol is effective in preventing and healing obesity, fatty liver and hypertriglyceridemia in mice fed with a high-fat diet, it inhibits tumor interstitial microvascular density and its proliferation activity, finally inhibits tumor growth, it also inhibits expression of VEGF and bFGF protein. (20R)-Protopanaxdiol has protective effect on myocardial ischemia, which may be related to improving free radicals metabolism and myocardial metabolism, decreasing plasma TXA 2 levels.|
|J Ginseng Res. 2015 Jan;39(1):61-8 |
|Molecular mechanism of protopanaxadiol saponin fraction-mediated anti-inflammatory actions.[Pubmed: 25535478]|
|Korean Red Ginseng (KRG) is a representative traditional herbal medicine with many different pharmacological properties including anticancer, anti-atherosclerosis, anti-diabetes, and anti-inflammatory activities. Only a few studies have explored the molecular mechanism of KRG-mediated anti-inflammatory activity.
METHODS AND RESULTS:
We investigated the anti-inflammatory mechanisms of the protopanaxadiol saponin fraction (PPD-SF) of KRG using in vitro and in vivo inflammatory models.
PPD-SF dose-dependently diminished the release of inflammatory mediators [nitric oxide (NO), tumor necrosis factor-α, and prostaglandin E2], and downregulated the mRNA expression of their corresponding genes (inducible NO synthase, tumor necrosis factor-α, and cyclooxygenase-2), without altering cell viability. The PPD-SF-mediated suppression of these events appeared to be regulated by a blockade of p38, c-Jun N-terminal kinase (JNK), and TANK (TRAF family member-associated NF-kappa-B activator)-binding kinase 1 (TBK1), which are linked to the activation of activating transcription factor 2 (ATF2) and interferon regulatory transcription factor 3 (IRF3). Moreover, this fraction also ameliorated HCl/ethanol/-induced gastritis via suppression of phospho-JNK2 levels.
These results strongly suggest that the anti-inflammatory action of PPD-SF could be mediated by a reduction in the activation of p38-, JNK2-, and TANK-binding-kinase-1-linked pathways and their corresponding transcription factors (ATF2 and IRF3).
|Journal of Chinese Pharmaceutical Sciences, 2002, 37(2):100-3. |
|Antimyocardial ischemic effects of Panax quinquefolium 20s-protopanaxdiol saponins (PQDS) and its mechanism[Reference: WebLink]|
|To study the antimyocardial ischemic effects of Panax quinquefolium 20 s-protopanaxdiolsaponins (PQDS) extracted from the leaves of Panax quinquefolium and its mechanism. |
METHODS AND RESULTS:
The changes of myocardial infarct size, the serum creatine phosphokinase(CK), lactate dehydrogenase (LDH), superoside dismutase(SOD), catalase(CAT) and glutathione peroxidase(GSH-Px) activity, the serum lipid peroxidation(LPO) and myocardial free fatty acid(FFA), lactic acid(LA) content and plasma prostacycline(PGI2) and thromboxane (TXA2) level were determined in rats with acute myocardial infarct model induced by ligating the left anterior descending coronary artery(LAD). After treated by PQDS(in a dosage of 12.5~50 mg · kg-1 iv at the same time of operation and 6 h later), the sizes of acute myocardial infarction were significantly reduced. The serum CK, LDH activity, the plasma TXA2 levels and myocardial FFA and LA contents were declined, while PGI2/TXA2 was increased significantly. In addition, serum LPO content was declined, SOD, CAT and GSH-Px levels were increased markedly.
PQDS had protective effect on myocardial ischemia, which may be related to improving free radicals metabolism and myocardial metabolism, decreasing plasma TXA2 levels. Therefore, PQDS may be an effective drug for the treatment of myocardial ischemia.