Ganoderma lucidum protects from dopaminergic neuron degeneration.
Parkinson's disease (Prevention)
Reishi (Health aspects)
Nervous system (Degeneration)
Nervous system (Prevention)
|Publication:||Name: Australian Journal of Medical Herbalism Publisher: National Herbalists Association of Australia Audience: Academic Format: Magazine/Journal Subject: Health Copyright: COPYRIGHT 2009 National Herbalists Association of Australia ISSN: 1033-8330|
|Issue:||Date: Winter, 2009 Source Volume: 21 Source Issue: 4|
|Geographic:||Geographic Scope: Australia Geographic Code: 8AUST Australia|
Zhang R, Xu S, Cai Y, Zhou M, Zuo X, Chan P. 2009. Ganoderma
lucidum protects dopaminergic neuron degeneration through inhibition of
microglial activation. eCAM. Advance Access published online on July 16,
Parkinson's disease is a neurodegenerative condition that impairs the motor functioning of the sufferer resulting in tremors, muscle rigidity and a slowing or loss of physical movement. There is evidence to suggest that neuronal inflammation plays a role in the pathogenesis of Parkinson's disease. If activated, microglia (the innate immune cells of the central nervous system) play key roles in the progressive neurodegeneration of this disease. The neurotoxic and inflammatory mediators they produce can deplete the antioxidant of dopaminergic neurons, impair mitochondrial function, inhibit the re-uptake of glutamate and initiate CNS tissue damage. This makes microglia a promising target for preventative therapy and to slow or halt progression of the condition.
Lingzhi or reishi mushroom (Ganoderma lucidum) (GL) has been widely used as a medicinal agent in China for over 1000 years. Previous studies have demonstrated anti-inflammatory, antioxidant and immunomodulary activity, along with an ability to promote mitochondrial energy production. It has been shown to prevent neuronal loss following cerebral ischemia, sparking speculation that it may have other neuroprotective roles.
The researchers in this study set out to determine whether the mushroom could also protect against dopaminergic neuron degeneration and attenuate microgial inflammatory responses to endogenous or exogenous stimulus. The GL extracts used were prepared from the fruiting body with methanol and contained mainly polysaccharides and ergosterin. Microglial cells isolated and purified from the brains of Wistar rats were cultured in the laboratory and subjected to various experiments in which they were treated with the mushroom extracts at dosages varying from 50-400 ug/mL and exposed to lipopolysaccharide or cell membrane fractions treated with 1-methyl-4-phenylpyridinium (MPP+).
It was found that GL prevented the production of proinflammatory cytokines and reactive oxygen species by microglia, protected against MPP+ and LPS induced dopaminergic neurodegeneration in the presence of microglia, and prevented the increased expression of TNF-[alpha] and IL-1[beta] mRNA by LPS and MPP+ treated membrane. All of these effects were dose dependent with highly significant differences affected by 400 ug/mL of GL extract.
These results provide very promising evidence that GL effectively protects dopaminergic neurons against inflammatory damage by activated microglia following LPS and MPP+ exposure. The mechanism appears to be the ability of the mushroom extract to reduce the production of inflammatory and toxic factors by microglial cells. Further studies on the extract are warranted.
Tessa Finney-Brown MNHAA
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