Parkinson's Disease Tulip


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Old 05-21-2010, 01:47 PM #1
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
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15 yr Member
reverett123 reverett123 is offline
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Join Date: Aug 2006
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Default White Rat Report: Chinese Skullcap (not American)

Scutellaria baicalensis is the big brother to American skullcap. It has been on my "to test" list for a long time and I started yesterday. So this is very preliminary. But one thing has already surfaced - this stuff is an extremely effective anti-inflammatory and I have proven it more clearly than I expected. Let me explain-

I have a space between two of my molars that traps food. I have to keep at it constantly to keep it from getting very painful, i.e. inflamed. And because I am undisciplined the normal condition is sore to touch. Except that today there is no tenderness whatsoever. It has been well over a year since I have been like that. In truth I don't remember just when. Today I can poke it with my finger with no mercy and there is no pain.

I took a single capsule yesterday containing 200 mg of the root standardized to 34 mg baicalein and 0.8 mg wogonin. Brand "New Chapter".

I am not going to report on PD-related effects for a few days, but you might be interested in these reports:


1. J Neural Transm. 2005 Mar;112(3):331-47. Epub 2004 Oct 22.

Inhibition of microglial activation by the herbal flavonoid baicalein attenuates
inflammation-mediated degeneration of dopaminergic neurons.

Li FQ, Wang T, Pei Z, Liu B, Hong JS.

Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National
Institute of Environmental Health Sciences, Research Triangle Park, NC 27709,
USA.

Accumulating evidence has suggested that inflammation in the brain participates
in the pathogenesis of Parkinson's disease (PD). Therefore, anti-inflammatory
therapy has attracted much attention as novel interference to neurodegenerative
diseases. Baicalein, a major flavonoid extracted from a traditional Chinese herb
Scutellaria baicalensis Georgi (Huangqin), possesses potent anti-inflammatory and
antioxidant properties. To test the potential neuroprotective effect of baicalein
on dopaminergic neurons, primary midbrain neuron-glia cultures from E-14 rat
embryos were used. Cultures were pretreated with baicalein for 30 min prior to
stimulation with lipopolysaccharide (LPS, 10 ng/ml). LPS leads to massive
activation of microglial cells revealed by OX-42 immunostaining, and produced
excessive quantities of NO. Excessive elevation of superoxide level was also
observed in enriched-microglia after stimulating with LPS. LPS-induced damage to
dopaminergic neurons was evaluated by uptake capacity for [3H]dopamine and
tyrosine hydroxylase (TH)-immunocytochemistry. Pretreatment with baicalein
concentration-dependently attenuated LPS-induced decrease in [3H]dopamine uptake
and loss of TH-immunoreactive (TH-ir) neurons, which the maximum protective
effect was observed at the concentration of 5 microM. Post-treatment with
baicalein (5 microM) was also shown to be effective even if baicalein
administered up to 2 h later than LPS application. Morphological study shows that
baicalein (5 microM) almost completely blocked LPS-induced activation of
microglia. Excessive production of TNF(alpha) and free radicals such as NO and
superoxide by LPS stimulation were also attenuated by baicalein at a
concentration-dependent pattern. The present study indicates that baicalein
exerts potent neuroprotective effect on LPS-induced injury of dopaminergic
neurons. We hypothesize that the inhibition of LPS-induced production of NO and
free radicals from microglia may underlie the mechanism of baicalein's
neuroprotection.

PMID: 15503194 [PubMed - indexed for MEDLINE]


1. J Neural Transm. 2005 Mar;112(3):331-47. Epub 2004 Oct 22.

Inhibition of microglial activation by the herbal flavonoid baicalein attenuates
inflammation-mediated degeneration of dopaminergic neurons.

Li FQ, Wang T, Pei Z, Liu B, Hong JS.

Neuropharmacology Section, Laboratory of Pharmacology and Chemistry, National
Institute of Environmental Health Sciences, Research Triangle Park, NC 27709,
USA.

Accumulating evidence has suggested that inflammation in the brain participates
in the pathogenesis of Parkinson's disease (PD). Therefore, anti-inflammatory
therapy has attracted much attention as novel interference to neurodegenerative
diseases. Baicalein, a major flavonoid extracted from a traditional Chinese herb
Scutellaria baicalensis Georgi (Huangqin), possesses potent anti-inflammatory and
antioxidant properties. To test the potential neuroprotective effect of baicalein
on dopaminergic neurons, primary midbrain neuron-glia cultures from E-14 rat
embryos were used. Cultures were pretreated with baicalein for 30 min prior to
stimulation with lipopolysaccharide (LPS, 10 ng/ml). LPS leads to massive
activation of microglial cells revealed by OX-42 immunostaining, and produced
excessive quantities of NO. Excessive elevation of superoxide level was also
observed in enriched-microglia after stimulating with LPS. LPS-induced damage to
dopaminergic neurons was evaluated by uptake capacity for [3H]dopamine and
tyrosine hydroxylase (TH)-immunocytochemistry. Pretreatment with baicalein
concentration-dependently attenuated LPS-induced decrease in [3H]dopamine uptake
and loss of TH-immunoreactive (TH-ir) neurons, which the maximum protective
effect was observed at the concentration of 5 microM. Post-treatment with
baicalein (5 microM) was also shown to be effective even if baicalein
administered up to 2 h later than LPS application. Morphological study shows that
baicalein (5 microM) almost completely blocked LPS-induced activation of
microglia. Excessive production of TNF(alpha) and free radicals such as NO and
superoxide by LPS stimulation were also attenuated by baicalein at a
concentration-dependent pattern. The present study indicates that baicalein
exerts potent neuroprotective effect on LPS-induced injury of dopaminergic
neurons. We hypothesize that the inhibition of LPS-induced production of NO and
free radicals from microglia may underlie the mechanism of baicalein's
neuroprotection.

PMID: 15503194 [PubMed - indexed for MEDLINE]


1. Clin Mol Allergy. 2007 Nov 26;5:5.

Baicalein inhibits IL-1beta- and TNF-alpha-induced inflammatory cytokine
production from human mast cells via regulation of the NF-kappaB pathway.

Hsieh CJ, Hall K, Ha T, Li C, Krishnaswamy G, Chi DS.

Departments of Internal Medicine, James H, Quillen College of Medicine, East
Tennessee State University, Johnson City, Tennessee 37614, USA. chi@etsu.edu.

ABSTRACT: BACKGROUND: Human mast cells are multifunctional cells capable of a
wide variety of inflammatory responses. Baicalein (BAI), isolated from the
traditional Chinese herbal medicine Huangqin (Scutellaria baicalensis Georgi),
has been shown to have anti-inflammatory effects. We examined its effects and
mechanisms on the expression of inflammatory cytokines in an IL-1beta- and
TNF-alpha-activated human mast cell line, HMC-1. METHODS: HMC-1 cells were
stimulated either with IL-1beta (10 ng/ml) or TNF-alpha (100 U/ml) in the
presence or absence of BAI. We assessed the expression of IL-6, IL-8, and MCP-1
by ELISA and RT-PCR, NF-kappaB activation by electrophoretic mobility shift assay
(EMSA), and IkappaBalpha activation by Western blot. RESULTS: BAI (1.8 to 30 muM)
significantly inhibited production of IL-6, IL-8, and MCP-1 in a dose-dependent
manner in IL-1beta-activated HMC-1. BAI (30 muM) also significantly inhibited
production of IL-6, IL-8, and MCP-1 in TNF-alpha-activated HMC-1. Inhibitory
effects appear to involve the NF-kappaB pathway. BAI inhibited NF-kappaB
activation in IL-1beta- and TNF-alpha-activated HMC-1. Furthermore, BAI increased
cytoplasmic IkappaBalpha proteins in IL-1beta- and TNF-alpha-activated HMC-1.
CONCLUSION: Our results showed that BAI inhibited the production of inflammatory
cytokines through inhibition of NF-kappaB activation and IkappaBalpha
phosphorylation and degradation in human mast cells. This inhibitory effect of
BAI on the expression of inflammatory cytokines suggests its usefulness in the
development of novel anti-inflammatory therapies.

PMCID: PMC2206049
PMID: 18039391 [PubMed - in process]
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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