Thunder God Vine
Scientific Name(s): Tripterygium wilfordii Hook. Family: Celastraceae
Common Name(s): Lei-kung t'eng , lei gong teng (Chinese), thunder god vine , huang-t'eng ken (yellow vine root), tsao-ho-hua (early rice flower)
Clinical Overview
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Uses of Thunder God Vine
Thunder god vine has antifertility properties, primarily acting on sperm development (eg, sperm head-tail separation), other than affecting testosterone levels. 1 , 2 In clinical trials it has been effective in treating autoimmune disease. Thunder god vine has shown antiviral and antitumor activity, but no clinical trials are available.
Thunder God Vine Dosing
An extract of thunder god vine was used in a trial for rheumatoid arthritis at a dose of 180 to 360 mg/day. 3
Contraindications
Contraindications have not yet been determined.
Pregnancy/Lactation
Information regarding safety and efficacy in pregnancy and lactation is lacking.
Thunder God Vine Interactions
None well documented.
Thunder God Vine Adverse Reactions
Side effects include gastrointestinal upset, infertility, suppression of white blood cells, amenorrhea, and one fatality.
Toxicology
Little information about lethal toxicities has been reported.
Botany
Tripterygium is a perennial twining vine that grows in southern China, usually close to water sources. It is native to the Hunan province. It has reddish-brown branches with oval leaves. In the summer, small white terminal flowers bloom. 1
History
The thunder god vine has been used for centuries in traditional Chinese medicine to treat fever, boils, abscesses, and inflammation. It has also been put to use as an insecticide to kill maggots or larvae and as a rat and bird poison. 1
Chemistry
Triterpene compounds (eg, tripterygone) have been isolated from thunder god vine roots. 4 A nortriterpenoid has also been isolated. 5 An anti-HIV constituent, neotripterifordin, has been recently identified. 6 Six diterpene epoxides have been identified, and listed as triptolide, tripdiolide, triptolidenol, tripchlorolide, 16-hydroxytriptolide. 7 , 8
Thunder God Vine Uses and Pharmacology
Pharmacology of thunder god vine includes reports in the areas of antifertility, autoimmune disease, antiviral, antitumor, and other effects.
AntifertilityAnimal data
Research reveals little or no animal data regarding antifertility uses with this product.
Clinical dataDuring the late 1980s and early 1990s, human studies evaluating thunder god vine for rheumatoid arthritis and psoriasis treatment revealed an unexpected side effect in male subjects. It was discovered that thunder god vine had reversible effects on sperm production and motility. This suggested the plant's use as a possible male antifertility drug. 1 A number of thunder god vine constituents are responsible for these potent antifertility actions, including triptolide and tripdiolide. 9 One report identified 6 compounds of the plant with antifertility effect in mice. 10 A later report confirms the 6 antifertility compounds in both rats and man. These compounds act primarily on sperm development (eg, sperm head-tail separation), rather than affecting testosterone levels. 1 , 2 Fertility is reversible after termination of administration of thunder god vine preparations. Sperm returned to normal 6 weeks later. 2 A review of thunder god vine's fertility regulatory effects is available. 11
The effective antifertility dose is 1/3 the recommended dose for treatment of arthritis or skin diseases. 12
One report compared 1 thunder god vine constituent to gossypol, finding inhibition of spermatogenesis, turnover of basic nuclear protein in late elongated spermatids and head-tail separation (among other antifertility effects) to be more pronounced in the thunder god vine constituent than in gossypol. 11
Autoimmune diseaseThunder god vine has been reported to be effective in treating autoimmune diseases in in vitro models and in animal and human studies.
In vitro, immunosuppressive activity was shown to be caused by the constituents tripchlorolide and tribromolide. 13 Another report analyzes T2 (a chloroform methanol extract of the plant) and an ethyl acetate extract, both of which contained triptolide and tripdiolide as the major immunosuppressive diterpenoids. 14 A new immunosuppressive component, phenolic nortriterpene demethylzeylasteral, has been identified. 15
In vitro analysis indicates thunder god vine inhibits transcription of the cytokine genes IL2 and gamma interferon. 16 The plant is also capable of inhibiting several other immune functions in vitro, including response of human mononuclear cells and generation of cytotoxic T-cells. 17 Another report measures ability of thunder god vine to affect cytokine secretion from monocytes or T-cells, prostaglandin E2 secretion from monocytes and other parameters of immune response. Results confirmed powerful suppressive effects in vitro, suggesting its use in rheumatic disease. 18 A similar study examining the mechanism of thunder god vine's effectiveness in rheumatoid arthritis isolated human peripheral blood mononuclear cells, then separated them into monocytes, T-cells, and B-cells. Thunder god vine alcoholic extract inhibited T-cell and B-cell proliferation, IL2 production by T-cells, and immunoglobulin production by B-cells. 19 Peripheral blood mononuclear cells from rheumatoid arthritic patients and control patients were studied for effects of thunder god vine polyglycosides. The thunder god vine preparation was found to act on both monocytes and lymphocytes, again confirming the immunosuppressive activity of the plant. 20
Animal dataIn mice, thunder god vine isolate triterene inhibited antibody response and inhibited granuloma growth in rats. 21 Also in rodents, results of another report indicated six diterpenes (triptolide, tripchlorolide, triptonide, tripdiolide, triptolidenol, and 16-hydroxytriptolide) all to possess anti-inflammatory and immunosuppressive actions in vivo. The constituent triptriolide had anti-inflammatory activity only. 22 A thunder god vine isolate in different concentrations was studied for its anti-inflammatory effects. It markedly inhibited vascular permeability in mice, inhibited hind paw edema and also inhibited proliferation of granuloma, suggesting the isolate's ability to stimulate pituitary-adrenal axis. 23 In another report, it was suggested that the suppressive effect of thunder god vine may be mediated by substance P, when studied in rat spinal dorsal horn. 24
Clinical dataHuman clinical trials evaluating the beneficial effects of thunder god vine preparations to treat autoimmune diseases are very promising. An analysis of 165 cases of thunder god vine's actions on rheumatoid arthritis is available. 25 Later reports confirm the plant's efficacy, as well. In a prospective, controlled double-blind crossover study in 70 rheumatoid arthritis patients, polyglycoside constituent “T2” from thunder god vine had “impressive, curative effects.” 26 Multi-glycosides of TGV, 30 mg/day, in 32 rheumatoid arthritis patients, resulted in significant improvements in clinical and laboratory variables. 27 Oral tablets containing thunder god vine had obvious “anti-inflammatory, analgesia and immunosuppressive actions” in both standard and sustained release forms, when evaluated in a 226-patient, prospective, multi-center study. 28
AntiviralNeotripterifordin has been found to show potent anti-HIV replication activity in vitro. 6 , 29 Triptofordin C-2 and other sesquiterpene components of thunder god vine, have been evaluated for their antiviral activity including human cytomegalovirus. 30
Animal/Clinical dataResearch reveals little or no data regarding antiviral uses of this product.
AntitumorAnimal data
It has been demonstrated that low doses of the diterpene triptolide isolate from thunder god vine possesses antileukemic activities in rodents 31 Additionally, it shows marked antitumor activity in mice. 31 , 32 Demethylzeylasteral, a nortriterpenoid isolate of thunder god vine, inhibits proliferation of vascular endothelial cells 30 times more effectively than the proliferation of human tumor cells, suggesting use in treating highly vascularized and metastatic tumors. 5 Effects of thunder god vine on tumor necrosis factor have been reported. 33
Clinical dataResearch reveals little or no clinical data regarding antitumor use with this product.
Other usesOther effects studied on thunder god vine include therapeutic actions in 12 cases of menorrhagia 34 and as treatment for multiple sclerosis. 35 A review is available on clinical uses of thunder god vine. 36
Dosage
An extract of thunder god vine was used in a trial for rheumatoid arthritis at a dose of 180 to 360 mg/day. 3
Pregnancy/Lactation
Information regarding safety and efficacy in pregnancy and lactation is lacking.
Interactions
None well documented.
Adverse Reactions
Gastrointestinal upset, infertility and suppression of lymphocyte proliferation are the usual side effects of thunder god vine. 37 Rash symptoms and alimentary canal incidences were experienced in one report, more so with a higher dose of the drug than with a lower dose. 27 Similarly, adverse reactions from a sustained release formulation of thunder god vine was approximately 20% in 226 rheumatoid arthritis patients, as opposed to a 70% side effect rate from standard release tablets. 28
Fourteen female rheumatoid arthritis patients developed amenorrhea after treatment with “T2” (thunder god vine extract), suggesting its site of action to be the ovary. These effects were reversible after discontinuation of the drug. 38
Toxicology
The triptolide constituent of thunder god vine exhibited non-specific cytotoxicity in cultured mammalian cell lines. Treatments of 50 mcg/mouse 3 times weekly in one preparation were lethal. 31
Little information about lethal toxicities has been reported; however, one case report describes an incidence of death (in a seemingly young and healthy male) 3 days post-ingestion of the drug. Later investigation found some incidence of coexisting cardiac damage. Prior to death, the patient experienced profuse vomiting, diarrhea, leukopenia, renal failure, hypotension, and shock. 37
Bibliography
1. Jones C. Herbs for Health . 1998 Jan/Feb:25.2. Zhen Q, et al. Contraception . 1995;51(2):121–29.
3. Tao X, et al. Arthritis Rheum . 2002;46:1735-43.
4. Zhang D, et al. Yao Hsueh Hsueh Pao . 1991;26(5):341–44.
5. Ushiro S, et al. Int J Cancer . 1997;72(4):657–63.
6. Chen K, et al. Bioorg Med Chem . 1995;3(10):1345–48.
7. Gu W, et al. Int J Immunopharmacol . 1995;17(5):351–56.
8. Ma P, et al. Yao Hsueh Hsueh Pao . 1991;26(10):759–63.
9. Matlin S, et al. Contraception . 1993;47(4):387–400.
10. Zheng J. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1991;13(6):398–403.
11. Qian S. Contraception . 1987;36(3):335–45.
12. Lu Q. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1990;12(6):440–44.
13. Yu D, et al. Yao Hsueh Hsueh Pao . 1992;27(11):830–36.
14. Tao X, et al. J Pharmacol Exp Ther . 1995;272(3):1305–12.
15. Tamaki T, et al. Transplant Proc . 1996;28(3):1379–80.
16. Lipsky P, et al. Semin Arthritis Rheum . 1997;26(5):713–23.
17. Li X, et al. Transplantation . 1990;50(1):82–86.
18. Chang D, et al. J Rheumatol . 1997;24(3):436–41.
19. Tao X, et al. Arthritis Rheum . 1991;34(10):1274–81.
20. Ye W. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1990;12(3):217–22.
21. Zhang L, et al. Yao Hsueh Hsueh Pao . 1990;25(8):573–77.
22. Zheng J. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1991;13(6):391–97.
23. Zheng Y, et al. Chung Kuo Yao Li Hsueh Pao . 1994;15(6):540–43.
24. Liu Y, et al. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1995;17(4):269–73.
25. Yan B. Chung Hsi I Chieh Ho Tsa Chih . 1985;5(5):280–83.
26. Tao X, et al. Chin Med J . 1989;102(5):327–32.
27. Tao X, et al. Chung Hsi I Chieh Ho Tsa Chih . 1990;10(5):289–91.
28. Li R, et al. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih . 1996;16(1):10–13.
29. Chen K, et al. J Nat Prod . 1992;55(1):88–92.
30. Hayashi K, et al. J Antimicrob Chemother . 1996;37(4):759–68.
31. Shamon L, et al. Cancer Lett . 1997;112(1):113–17.
32. Xu J, et al. Chung Kuo Chung Hsi I Chieh Ho Tsa Chih . 1992;12(3):161–64.
33. Zeng X, et al. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1996;18(2):138–42.
34. Shu H, et al. J Tradit Chin Med . 1984;4(3):237–40.
35. Sun J. Chung Hsi I Chieh Ho Tsa Chih . 1988;8(2):87–89.
36. Chu W. Chung Hsi I Chieh Ho Tsa Chih . 1988;8(7):443–45.
37. Chou W, et al. Int J Cardiol . 1995;49(2):173–77.
38. Gu C. Chung Kuo I Hsueh Ko Hsueh Yuan Hsueh Pao . 1989;11(2):151–53.
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