[imark3000]

http://www.sciencedaily.com/releases...rkinson%27s%29

[GerryW]

People with COPD are also deficient in Nrf2 defenses, but sulforaphane from broccoli restores normal levels. Perhaps it might work in PD, too. In any case, it helps brain injury. http://www.ncbi.nlm.nih.gov/pubmed/19515491

[VICTORIALOU]

A little online investigation....From the Cogane makers website: http://www.phytopharm.co.uk/

"Our lead series of compounds, the Sapogenins (including Cogane™ and Myogane™), has the potential to be a new class of therapy for neurodegenerative diseases including Parkinson’s disease, amyotrophic lateral sclerosis (ALS) and glaucoma."

Now to define the Sapogenins we go to Wiki:

Sapogenins are the aglycones, or non-saccharide, portions of the family of natural products known as saponins. Sapogenins contain steroid or other triterpene frameworks as their key organic feature. For example, steroidal sapogenins like tiggenin, neogitogenin, and tokorogenin have been isolated from the tubers of Chlorophytum arundinacelum.[2]
The chemical structure of yamogenin,[1] a sapogenin found in fenugreek

Now, Fenugreek is familiar as an herb used in cooking and healing for centuries but the tuber mentioned above turns out to be an herb used in Indian healing and previously studied:
http://www.ncbi.nlm.nih.gov/pubmed/20564504.

It is more commonly known as moosli or safed moosli which is a misnomer as there are several different species of moosli (which all appear to contain sapogenins).
http://www.hort.purdue.edu/newcrop/C...fedmoosli.html

Both fenugreek and moosli can be obtained as herbs online.

When I read that the sagonenins contain steroid or other triterpene frameworks as their key organic feature, a bell went off in my head.
I just had read of another study or trial that was being done with
triterpene. So I looked and found this article:

http://medicalxpress.com/news/2012-0...parkinson.html
Powerful class of antioxidants may be potent Parkinson's treatment

"A class of antioxidants called synthetic triterpenoids blocked development of Parkinson's in an animal model that develops the disease in a handful of days, said Dr. Bobby Thomas, neuroscientist at the Medical College of Georgia at Georgia Health Sciences University and corresponding author of the study in the journal Antioxidants & Redox Signaling. Thomas and his colleagues were able to block the death of dopamine-producing brain cells that occurs in Parkinson's by using the drugs to bolster Nrf2, a natural antioxidant and inflammation fighter. Stressors from head trauma to insecticide exposure to simple aging increase oxidative stress and the body responds with inflammation, part of its natural repair process. "This creates an environment in your brain that is not conducive for normal function," Thomas said. "You can see the signs of oxidative damage in the brain long before the neurons actually degenerate in Parkinson's." Nrf2, the master regulator of oxidative stress and inflammation, is – inexplicably – significantly decreased early in Parkinson's. In fact, Nrf2 activity declines normally with age. "In Parkinson's patients you can clearly see a significant overload of oxidative stress, which is why we chose this target," Thomas said. "We used drugs to selectively activate Nrf2." They parsed a number of antioxidants already under study for a wide range of diseases from kidney failure to heart disease and diabetes, and found triterpenoids the most effective on Nrf2. Co-author Dr. Michael Sporn, Professor of Pharmacology, Toxicology and Medicine at Dartmouth Medical School, chemically modified the agents so they could permeate the protective blood-brain barrier. Both in human neuroblastoma and mouse brain cells they were able to document an increase in Nrf2 in response to the synthetic triterpenoids. Human dopaminergic cells are not available for research so the scientists used the human neuroblastoma cells, which are actually cancer cells that have some properties similar to neurons. Their preliminary evidence indicates the synthetic triterpenoids also increase Nrf2 activity in astrocytes, a brain cell type which nourishes neurons and hauls off some of their garbage. The drugs didn't protect brain cells in an animal where the Nrf2 gene was deleted, more proof that that Nrf2 is the drugs' target. The researchers used the powerful neurotoxin MPTP to mimic Parkinson's-like brain cell damage in a matter of days. They are now looking at the impact of synthetic triterpenoids in an animal model genetically programmed to acquire the disease more slowly, as humans do. Collaborators at Johns Hopkins School of Medicine also will be providing induced pluripotent stem cells, adult stem cells that can be coaxed into forming dopaminergic neurons, for additional drug testing."

So, personally, as a lab rat myself, and desperate, I'm not waiting for Pharma to go through their machinations before I give it a try.

[wxxu]

Baicalein protects against 6-OHDA-induced neurotoxicity through activation of Keap1/Nrf2/HO-1 and involving PKCα and PI3K/AKT signalling pathways

http://pubs.acs.org/doi/abs/10.1021/jf301511m

Abstract
Baicalein, one of the major flavonoids found in Scutellaria baicalensis Georgi, displays neuroprotective effects on experimental models of Parkinson’s disease (PD) in vitro and in vivo. Although the anti-oxidative and/or anti-inflammatory activity of baicalein likely contributes to these neuroprotective effects, other modes of action remain largely uncharacterized. In the present study, baicalein pre-treatment significantly prevented cells from 6-hydroxydopamine (6-OHDA)-induced damage by attenuating cellular apoptosis. However, post-treatment with baicalein did not show any restorative effect against 6-OHDA induced cellular damage. We found that baicalein increased transcriptional factor NF-E2-related factor 2 (Nrf2)/hemo oxygenase 1(HO-1) protein expression and decreased Kelch-like ECH-associated protein 1 (Keap1) in a time- and concentration-dependent manner in PC12 cells. In addition, baicalein induced Nrf2 nuclear translocation, and enhanced anti-oxidant response element (ARE) transcriptional activity, which conferred cytoprotection against 6-OHDA-induced oxidative injury. Moreover, we demonstrated that cytoprotective effects of baicalein could be attenuated by Nrf2 siRNA transfection and the HO-1 inhibitor zinc protoporphyrin (Znpp), as well as the proteasome inhibitor MG132. Furthermore, PKCα and AKT protein phosphorylation were upregulated by baicalein pre-treatment, and selective inhibitors targeted to PKC, PI3K and AKT could block the cytoprotective effects of baicalein. Taken together, our results indicate that baicalein prevented PC12 cells from 6-OHDA-induced oxidative damage via the activation of Keap1/Nrf2/HO-1, and it also involves the PKCα and PI3K/AKT signalling pathway. Ultimately, the neuroprotective effects of baicalein may endue baicalein as a promising candidate for the prevention of PD.

[lurkingforacure]

Originally Posted by wxxu

Baicalein protects against 6-OHDA-induced neurotoxicity through activation of Keap1/Nrf2/HO-1 and involving PKCα and PI3K/AKT signalling pathways

http://pubs.acs.org/doi/abs/10.1021/jf301511m

Abstract
Baicalein, one of the major flavonoids found in Scutellaria baicalensis Georgi, displays neuroprotective effects on experimental models of Parkinson’s disease (PD) in vitro and in vivo. Although the anti-oxidative and/or anti-inflammatory activity of baicalein likely contributes to these neuroprotective effects, other modes of action remain largely uncharacterized. In the present study, baicalein pre-treatment significantly prevented cells from 6-hydroxydopamine (6-OHDA)-induced damage by attenuating cellular apoptosis. However, post-treatment with baicalein did not show any restorative effect against 6-OHDA induced cellular damage. We found that baicalein increased transcriptional factor NF-E2-related factor 2 (Nrf2)/hemo oxygenase 1(HO-1) protein expression and decreased Kelch-like ECH-associated protein 1 (Keap1) in a time- and concentration-dependent manner in PC12 cells. In addition, baicalein induced Nrf2 nuclear translocation, and enhanced anti-oxidant response element (ARE) transcriptional activity, which conferred cytoprotection against 6-OHDA-induced oxidative injury. Moreover, we demonstrated that cytoprotective effects of baicalein could be attenuated by Nrf2 siRNA transfection and the HO-1 inhibitor zinc protoporphyrin (Znpp), as well as the proteasome inhibitor MG132. Furthermore, PKCα and AKT protein phosphorylation were upregulated by baicalein pre-treatment, and selective inhibitors targeted to PKC, PI3K and AKT could block the cytoprotective effects of baicalein. Taken together, our results indicate that baicalein prevented PC12 cells from 6-OHDA-induced oxidative damage via the activation of Keap1/Nrf2/HO-1, and it also involves the PKCα and PI3K/AKT signalling pathway. Ultimately, the neuroprotective effects of baicalein may endue baicalein as a promising candidate for the prevention of PD.

I hate to be the party-pooper, but this is yet another study where they give the compound BEFORE causing PD-ish damage. IMHO, this does not help us! No one has the luxury of getting whatever the test subject compound is before they get PD, so why do researchers keep structuring studies this way? They actually admit in this study that taking the compound AFTER damage has been caused has no beneficial effect, which is virtually the situation with everyone with PD, so what is the point? Please tell me I am missing something, it's just that I have read so very many studies structured like this and dont understand the goal when it varies so much from real PD life.

[wxxu]

Originally Posted by lurkingforacure

I hate to be the party-pooper, but this is yet another study where they give the compound BEFORE causing PD-ish damage. IMHO, this does not help us! No one has the luxury of getting whatever the test subject compound is before they get PD, so why do researchers keep structuring studies this way? They actually admit in this study that taking the compound AFTER damage has been caused has no beneficial effect, which is virtually the situation with everyone with PD, so what is the point? Please tell me I am missing something, it's just that I have read so very many studies structured like this and dont understand the goal when it varies so much from real PD life.

It may help those neurons that have not died and are still struggling... Plus this herb has a long lasting popularity in China and Asia, so it maybe relatively safer for us to try. From my own experience with baicalein in less a month, it has so far eased the tremor noticeably and has no noted side effect.

[bubblyshar]

Hi there, Can you tell me what this herb is? I want to get it for my Dad. He has tremors in his hands.

Thanks!

Originally Posted by wxxu

It may help those neurons that have not died and are still struggling... Plus this herb has a long lasting popularity in China and Asia, so it maybe relatively safer for us to try. From my own experience with baicalein in less a month, it has so far eased the tremor noticeably and has no noted side effect.

[VICTORIALOU]

What is saponin, the red ginseng component?

Saponin derives from a Greek word Sapona, meaning soap. The name Sapona went through a suffix change and was given due to the micro bubbles that appear from the solution.

Generally the saponin component lowers water’s surface tension and easily causes bubbles, and there are many plants around us that contain saponin.

Bean, green onion, deodeok, bellflower root, water parsley, mung bean, garlic, onion, ginkgo nut, arrowroot, leek, and many other plants contain a small amount of saponin, but saponin in red ginseng is strictly different from these.


The red ginseng saponin has mild medicinal characteristics with no toxins, almost no hemolytic characters, and is completely different from saponin found in other plants in its chemical makeup.

In order to differentiate the red ginseng saponin from saponin found in other plants, it was given the name ginsenoside, meaning glycoside from ginseng.

Saponin found in plants are categorized into 3 groups of protopanaxadiol (PD), protopanaxatrio (PT), and oleanolic acid (OA).

Most saponin found in plants are the oleanane type, while saponin found in red ginseng is the triterpenoid saponin of the dammarane group, which is rarely found in plants.

Ginsenoside’s key medical benefits reach out to the central nerve system, endocrine system, immune system, metabolism, and etc. and have various effect on the body’s conditioning function.


General features are:

1. Melts well in water and alcohol;

2. Continues to create bubbles;

3. Has physiological detoxification capabilities, and it has been revealed that ginseng saponin is very mild and does not have toxic effect from overdose.

Simply put, it would be easier to understand to say that saponin enters the body and cleans the vessels and various organs as if it were cleaned with soap.

Ginseng contains 24 types of saponin, while red ginseng contains 32 types.



The key medicinal components of ginseng is known to be the 30 or so types of saponin (24 types in white ginseng, 32 types in red ginseng), named ginsenoside. Thanks to the continued research efforts of renown scientists around the world, its chemical structure, as well as its medical vitality are being uncovered.

Benefits of saponin:

- Breaks down fat well, and accelerates nutrient absorption and digestion;

- Vitalizes enzymes within cells and improves metabolism;

- Increases energy, invigorates, fatigue recovery, improves limpness and lack of appetite.

- Improves serum protein synthesis


According to recent studies, such benefits of red ginseng intake are a result of red ginseng saponin and non-saponin components working together.


Of course, non-saponin components are also known to have benefits towards immunity improvement, blood sugar lowering, anti-cancer, and etc. However, it has been revealed that much of the broad physiologically vitalizing effects of red ginseng are centered around saponin.

[wxxu]

Originally Posted by bubblyshar

Hi there, Can you tell me what this herb is? I want to get it for my Dad. He has tremors in his hands.

Thanks!

Hi, I use "New Chapter" brand "Chinese Skullcap". Each capsule contents baicalein, baicalin and wogonin - three major flavonoids found in Chinese Skullcup. I took 1 capsule per day for about two weeks, then I increased to 2 capsules per day.

[bubblyshar]

thanks for this response. What change have you noticed by taking the chinese skullcap?

Thanks

Originally Posted by wxxu

Hi, I use "New Chapter" brand "Chinese Skullcap". Each capsule contents baicalein, baicalin and wogonin - three major flavonoids found in Chinese Skullcup. I took 1 capsule per day for about two weeks, then I increased to 2 capsules per day.