Tripterygium wilfordii - Thundergod Vine
Posted 08 August 2011 - 10:24 PM
There are currently a number of clinial trials running in western countries to establish efficacy in double blind studies. Some of these are in australia, including one in brisbane for psoriasis.
Triptolide appears to have a similar antiinflammatory effect to prednisone, but works on very different principles. It also does not have the dangerous side effects of prednisone on bone density and insulin levels.
My main interest in triptolide is the regulatory effect it has on autoreactive T cells, ie T cells that attack the tissues of the body by error. This is what drives conditions like psoriasis, psoriatic arthritis, rheumatoid arthritis, and a whole host of other inflammatory conditions. In my case there is a high likelihood that my GI problems are at least partially due to an autoimmune condition and as other autoreactive T cells conditions run in my family it seems a safe bet to target these first.
The main reason why I am documenting my experiments in this forum rather than the pharmacology forum is becuase I want this to be indexed by google. Research into Tripterygium wilfordii has been going on since the 90's, yet the data available online is very patchy. In particular I found it very difficult to find the actual dose for immunosuppressant treatment. Most articles simple refer to an ethyl acetate extract and then give the dosage in form of this extract. As I could only source one strength of extract from china I had almost decided that it must all be the same potency. This is however not the case. Obviously there have been advances in extraction techniques, because the extract available today is far more potent than the extract from the 90's. So much so that if you follow the instructions of consuming 360mg of extract you would be taking triple the LD50. OOOPS!
I had to buy 4 papers to track down the actual manufacturing method and hence the dosages used in those trials. So here is the summary:
Tripterygium wilfordii root is extracted consecutively into ethanol and then ethyl acetate. The extracts are combined and dried on starch.
The old extracts contained 9.9 microgram of triptolide [and others] per 30mg and was dosed in 30mg capsules.
The new extracts contain 0.5% triptolide [and others], which means to get 10 micrograms in a capsule you only need 2mg of the new extract. ie todays extract is 15 times as potent as the one used in all the literature.
All treatments start at 30mg extract [9.9micrograms triptolide] and are increased at 2 weeks intervals by a further 30mg extracts if there has not been sufficient response. For immunosuppressant activity doses of 180-570mg of the old extract are required.
For the new extract this would be 2mg to start with, increased by 2mg every 2 weeks up to 12mg which is the lower end of the 'high dose' regimen. The higher end of the high dose regimen would be 38mg of new extract.
I should also mention that ther eis a low dose regimen which is used for a completely unrelated purpose. At low doses the herb/extract will render sperm dead and/or immotile. Low doses will kill about 90% of sperm and will render the remainder immotile. As there are usually no side effect at the low doses, Tripterygium extracts can be used as male contraceptives.
The sperm killing activity is generally regarded as temporary, however there are some indications that very long use [years] and advancing age can cause a permanent reduction in sperm function.
Male infertility is also the main side effect listed for the high dose treatment. other side effects include headaches, digestive problems, liver toxicity and general immune reactions. Cessation of the supplement also stops the side effects.
There are other interesting aspects of this plant. It appears to protect rats that have a parkinsons-like condition from developing the disease and this appears to be by protecting the dopamine receptors.
Anyway, tonight I am taking my first 2mg of extract, ie 10 micrograms of triptolide. hopefully i've done my calculations right
I am not expecting any immediate results, so this will be a slow thread, but I will post updates when I escalate the dose [which I may do weekly rather than fortnightly]. I am not expecting much until i hit the 12mg mark.
Anyone else interested in playing with this let me know as I have plenty of the extract and would be happy to share at cost since it has a limited shelf life. Obviously I am not providing it for consumption and what you do with it would be entirely your own responsibility. This is a very dangerous herb and even after 30 odd hours of study I am still a little hesitant - less so now that I've finally worked out the dosage issues.
My Blog & Tradelist
Posted 08 August 2011 - 10:40 PM
A bird does not sing because it has an answer.
It sings because it has a song.
Posted 09 August 2011 - 02:31 AM
Triptolide Down-regulates COX-2 Expression and PGE2 Release by Suppressing the Activity of NF-κB and MAP kinases in Lipopolysaccharide-treated PC12 Cells.
Geng Y, Fang M, Wang J, Yu H, Hu Z, Yew DT, Chen W.
Department of Neurology, Sir Run Run Shaw Hospital, Medical College, Zhejiang University, Hangzhou, China.
As an active compound extracted from the Chinese herb Tripterygium wilfordii, triptolide (TP) was demonstrated to have potent antiinflammatory and immunosuppressive properties in previous studies. Recently, it has been shown that TP prevented the loss of dopaminergic neurons in the substantia nigra of rats in a model of Parkinson's disease, but little is known about the precise neuroprotective mechanism of TP. This study was designed to elucidate whether the neuroprotective effect of TP is partially based on its direct inhibition of inflammatory molecules by investigating the effects of TP on the expression of cyclooxygenase (COX)-2 and prostaglandin E2 (PGE2) related to the nuclear factor (NF)-κB pathway in lipopolysaccharide (LPS)-stimulated PC12 cells. The activation of related upstream molecules such as NF-κB, P38, extracellular signal-regulated kinase (ERK)1/2, and beta-alanyl-alpha-ketoglutarate transaminase (AKT), in PC12 cells were investigated by real time polymerase chain reaction (PCR), western blotting and enzyme-linked immunosorbent assay (ELISA). Our results showed that TP directly inhibited the expression of both mRNA and protein of COX-2 (p < 0.01), decreased PGE2 production (p < 0.01) in a dose-dependent manner, down-regulated NF-κB activity (p < 0.01), and significantly inhibited the phosphorylation of p38, ERK1/2 (p42/p44) and AKT in PC12 cells after LPS challenge. This suggests that the neuroprotective effects of TP may be partially mediated by direct inhibition of the expression of COX-2, activation of NF-κB, and phosphorylation of p38, ERK1/2 (p42/p44) and AKT proteins of neuronal cells.
My Blog & Tradelist
Posted 09 August 2011 - 09:28 AM
i might use this search as my log in gate to sab.
Posted 09 August 2011 - 01:38 PM
Tripterygium wilfordii, they typo made us though number 1 with Tripterygium wildfordii.
LOL, that's the spelling on the packet from the supplier. Didn't even notice that it was wrong because I did my searches via 'triptolide'. Thanks for pointing it out - will fix as there is no point being number one on something that's wrong ;)
My Blog & Tradelist
Posted 14 August 2011 - 05:37 PM
Posted 15 August 2011 - 01:08 AM
The only clear side effect I have experienced wasn't one that was expected. I found myself not wanting to go to bed at my normal bedtime. Simply not tired even 2 or 3 hours later. I was taking the stuff in the later parts of the day, so I switched to taking it in the mornings and that solved the problem. I seem to get a lot more stuff done even though i don't feel any better. I doubt there would be a connection, but it actually feels just like LDN.
My Blog & Tradelist
Posted 15 August 2011 - 07:58 PM
Stinging nettle isnt bad for inflammation any way.
Posted 07 November 2011 - 07:25 PM
Have you seen this recent review?
A Chinese herb Tripterygium wilfordii Hook F in the treatment
of rheumatoid arthritis: mechanism, eYcacy, and safety
Jun Bao · Sheng-Ming DaiRheumatol Int (2011) 31:1123–1129
Posted 13 November 2011 - 10:45 PM
edit: got the paper. reading it tomorrow.
My Blog & Tradelist
Posted 13 November 2011 - 11:17 PM
Obviously an out there treatment, but you never know ;P
Edited by Qhorakuna tantani, 13 November 2011 - 11:20 PM.
Posted 13 November 2011 - 11:31 PM
anyway, the trypterygium was interesting. it actually made me worse. Could have been coincidence so will try again soon and don't want to post too much about it till then.
My Blog & Tradelist
Posted 22 February 2012 - 01:25 PM
High-throughput screening of chemical libraries for modulators of gene promoter activity of HLA-B2705: environmental pathogenesis and therapeutics of ankylosing spondylitis.
J Rheumatol. 2011 Jun;38(6):1061-5
Authors: Zhao L, Liu CH, Yu D
OBJECTIVE: Ankylosing spondylitis (AS) is a highly heritable disease with HLA-B27 being the strongest susceptible gene. In order to survey the environmental triggers for arthritis development, we used a high-throughput technique to screen the effects of 12,264 chemicals on the HLA-B27 gene promoter.
METHODS: Promoter reporter transfectants 293T-HLA-B27 and HeLa-HLA-B27 were tested using robotics with 12,264 chemicals. Chemicals that modulated HLA-B27 promoter activity > 150% or < 40% were selected for further evaluation of IC50/EC50 and cell viability.
RESULTS: The primary screening using the 293T-HLA-B27 promoter reporter cell line yielded 5.1% hits that either suppressed (556 chemicals) or enhanced (68 chemicals) the HLA-B27 promoter activity. A secondary reconfirmation screening was carried out with these 624 candidates using HeLa-HLA-B27 promoter reporter cells under several different culture conditions. The yield of positive candidates was 130, of which 47 were derived from natural products. Based on the bio-information of those positive natural products, 21 chemicals were selected for analysis by dose-response IC50/EC50 experiments. Eight compounds showed potential pharmacological activities. Two suppressors are both derived from an herbal medicine (lei gong teng) that has been used for decades to treat immune diseases. The 6 activators all belonged to a group of chemicals known as flavonoids, widely distributed among dietary fruits and vegetables.
CONCLUSION: Several common dietary products that contain certain flavonoids might be environmental risk factors for AS; the Chinese traditional herb lei gong teng might be a potential drug for patients who are HLA-B27-positive. These results provide new research directions for the pathogenesis and therapeutics of AS.
PMID: 21459940 [PubMed - indexed for MEDLINE]
Posted 22 February 2012 - 01:27 PM
Determination of four pyridine alkaloids from Tripterygium wilfordii Hook. f. in human plasma by high-performance liquid chromatography coupled with mass spectrometry.
J Chromatogr B Analyt Technol Biomed Life Sci. 2011 Nov 15;879(30):3516-22
Authors: Cai MQ, Chen XH, He SW, OuYang XK, Jin MC
A novel liquid chromatography-atmospheric-pressure chemical ionization-mass spectrometry (LC-APCI/MS) method was developed and validated for the simultaneous determination of four sesquiterpene pyridine alkaloids (wilfortrine, wilfordine, wilforgine and wilforine) in human plasma. The chromatographic separation was performed on a Shim-pack XR-ODS column using an ammonium acetate buffer solution-acetonitrile in a gradient program. The detection was achieved by an ion trap mass spectrometry in the positive selected ion monitoring (SIM) mode. The method utilized acetonitrile as protein precipitation solvent and followed by solid-phase extraction (SPE). Calibration curves were linear for the four alkaloids over the range of 0.5-100.0 μg/L with the limits of quantification of 0.5 μg/L, while the method exhibited the recovery of 86.5-98.6%, intra- and inter-day RSDs of less than 8.2% and 12.8%, respectively. Methodology was validated in line with the EU requirements (Commission Decision 2002/657/EC). Results of incurred samples demonstrated excellent reproducibility. To our knowledge, this is the first analytical method for simultaneous determination of the four sesquiterpene pyridine alkaloids in plasma. The method was applicable to clinical pharmaceutical research of alkaloids in rheumatoid arthritis volunteer patients after oral administrations.
PMID: 21982911 [PubMed - indexed for MEDLINE]
Triptolide (TPL) inhibits global transcription by inducing proteasome-dependent degradation of RNA polymerase II (Pol II).
PLoS One. 2011;6(9):e23993
Authors: Wang Y, Lu JJ, He L, Yu Q
Triptolide (TPL), a key biologically active component of the Chinese medicinal herbTripterygium wilfordii Hook. f., has potent anti-inflammation and anti-cancer activities. Its anti-proliferative and pro-apoptotic effects have been reported to be related to the inhibition of Nuclear Factor κB (NF-κ and Nuclear Factor of Activated T-cells (NFAT) mediated transcription and suppression of HSP70 expression. The direct targets and precise mechanisms that are responsible for the gene expression inhibition, however, remain unknown. Here, we report that TPL inhibits global gene transcription by inducing proteasome-dependent degradation of the largest subunit of RNA polymerase II (Rpb1) in cancer cells. In the presence of proteosome inhibitor MG132, TPL treatment causes hyperphosphorylation of Rpb1 by activation of upstream protein kinases such as Positive Transcription Elongation Factor b (P-TEFb) in a time and dose dependent manner. Also, we observe that short time incubation of TPL with cancer cells induces DNA damage. In conclusion, we propose a new mechanism of how TPL works in killing cancer. TPL inhibits global transcription in cancer cells by induction of phosphorylation and subsequent proteasome-dependent degradation of Rpb1 resulting in global gene transcription, which may explain the high potency of TPL in killing cancer.
PMID: 21931633 [PubMed - indexed for MEDLINE]
Posted 04 March 2012 - 01:00 PM