8 torthaí
Oxidative stress is significant in the pathogenesis of cerebral ischemia. Panax quinquefolium 20(S)-protopanaxadiol saponins (PQDS) have been demonstrated to exhibit a variety of biological effects in the cardiovascular system as a result of their antioxidant properties. However, little is known
In this study, we investigated the cardioprotective effect of Panax quinquefolium 20(S)-protopanaxadiol saponins (PQDS) both in vivo and in vitro. An animal model of acute myocardial infarction was induced by permanent ligation of the left anterior descending coronary artery in Sparague Dawley rats.
BACKGROUND
The root of Panax notoginseng is traditionally used as an anti-hemorrhagic agent to promote blood circulation without causing "congealed" blood. Furthermore, the flower of P. notoginseng is a popular, traditional medicine taken daily for the preventing of hypertension and for reducing
OBJECTIVE
Compound K (C-K; 20-O-D-glucopyranosyl-20(S)-protopanaxadiol) is a novel ginsenoside metabolite formed by intestinal bacteria and does not occur naturally in ginseng. In this study, we investigated whether administration of C-K has protective effects on myocardial ischemia-reperfusion
Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is a well-known traditional Chinese herbal medicine. Ginsenosides, which are triterpene derivatives that contain sugar moieties, are the main active ingredients of ginseng. 20(S)-Ginsenoside Rg3, a triterpene glycoside which chemically
Ginsenoside Rb1 (Rb1), one of the most abundant protopanaxadiol-type ginsenosides, exerts excellent neuroprotective effects even though it has low intracephalic exposure.The present study aimed to elucidate the apparent contradiction between the Ginseng, one of the oldest traditional Chinese medicinal herbs, has been used widely in China and Asia for thousands of years. Ginsenosides extracted from ginseng, which is derived from the roots and rhizomes of Panax ginseng C. A. Meyer, have been used in China as an adjuvant in the treatment of
Microglial activation plays a pivotal role in the pathogenesis of various neurologic disorders, such as cerebral ischemia, Alzheimer's disease, and Parkinson's disease. Thus, controlling microglial activation is a promising therapeutic strategy for such brain diseases. In the present study, we found