Ginseng extract may offer brain protection: Study

13-Jan-2011 - Last updated on 13-Jan-2011 at 17:17 GMT

An active protein found in ginseng root shows signs of neuroprotective support against stroke, and may benefit other neurodegenerative diseases, according to new research.

Published in the Journal of Ethnopharmacology, the study assessed the effects of Ginsenoside Rb1 (GRb1) – an active protein component of the ginseng root – on a group of adult male rats one with ischemic stroke.

The research found that GRb1 significantly increased the number of neural stem cells – known as neural precursors cells – after ischemic stroke compared to rats not infused with GRb1.

“The present study demonstrates that GRb1 promotes the neural behavior recovery, […] and induces neurogenesis after cerebral ischemia,” said the researchers, led by Dr Qiong-Lan Yuan from Tongji University School of Medicine in China.

“These results provide new support for the neuroprotective effects of GRb1 against ischemic stroke, which may be potential therapeutic treatment for other neurodegenerative disease such as Alzheimer disease and Parkinson disease,” they added.

Ginseng

Ginseng (Panax quinquefolius), has been an important component of Chinese medicine for thousands of years, and is suggested to protect the brain from the effects of certain types of stroke.

Previous research has suggested that an the ginseng active component Ginsenoside Rb1(GRb1) has neuroprotective effects or for cerebral ischemia.

It has been suggested that there beneficial properties are due to their effects on brain-derived neurotrophic factor (BDNF) – a protein that helps to support the survival of existing neurons, and encourages the growth and differentiation of new neurons and in the brain. Whilst other studies have linked levels of caspase- 3 – a protein that plays a vital role in programmed cell death and has been shown to be elevated levels after certain cardiovascular events.

“Recently, a battery of studies has shown that BDNF is strongly involved in neurological recovery after cerebral ischemia,” said the researchers.

However, Dr Yuan and colleagues said that the underlying mechanism of this protective function is unclear.

“We assessed whether this neuroprotective effect of GRb1 was mediated by the levels of brain-derived neurotrophic factor (BDNF), by the levels of caspase-3 proteins, and by induced neurogenesis in rats following transient cerebral ischemia,” said the authors.

Study details

The mechanism of GRb1 neuroprotection was evaluated by observing expressions of BDNF and caspase-3 and neurogenesis in rats with experimental cerebral ischemia.

Results revealed the GRb1 infusion after cerebral ischemia significantly promoted recoveries of neurological functions at three and five days post-stroke compared to ischemic rats not infused with GRb1.

They reported that BDNF levels were significantly increased in GRb1-treated rats, whilst infusion with GRb1 post- stroke was shown to significantly reduce levels of caspase-3 compared to control rats.

Mechanism

Yuan and colleagues said that the findings of the study indicate that regulation of the expressions of BDNF and caspase-3 may be involved in GRb1-induced neuroprotection against cerebral ischemia.

“GRb1 infusion after cerebral ischemia significantly inhibited caspase-3 activity at different time points. This is, to our knowledge, the first report that GRb1 inhibits caspase-3 in cerebral ischemia,” said the researchers.

“It is [also] the first time to show that GRb1 is capable of increasing BDNF expression after stroke … The increased BDNF expression may explain partly the neurological functional recovery after cerebral ischemia with GRb1 treatment,” they added.

However they added that the underlying mechanism by which GRb1 promotes functional recovery after stroke is still not completely clear.

Next questions

“Perhaps the most important questions in next study are to assess whether neural precursors cells differentiate into neurons with appropriate regional specificity after cerebral ischemia,” said Yuan and co- workers.

They explained that if the new neurons are capable of long-term survival and integration, then GRb1-induced neurogenesis is a plausible strategy for many other neurodegenerative disorders besides cerebral ischemia.

Source: Journal of Ethnopharmacology
Volume 132, Issue 2, Pages 393-39, doi: 10.1016/j.jep.2010.07.033
“Ginsenoside Rb1 regulates the expressions of brain-derived neurotrophic factor and caspase-3 and induces neurogenesis in rats with experimental cerebral ischemia”
Authors: X.Q. Gao, C.X. Yang, G.J. Chen, G.Y. Wang, B. Chen, S.K. Tan, J. Liu, Q.L. Yuan