Scientific Names: Tripterygii Wilfordii, Tripterygium wilfordii Hook. f.

Common Names: Lei Gong Teng, Thunder God Vine, Three-wing Nut, Huang Gen Teng, Huang Yao, Duan Chang Cao, Huang Teng Mu, Hong Yao, Huang Teng Cao.


The Chinese herb, Lei Gong Teng, comes from the roots, leaves and flowers of the tripterygium wilfordii Hook. f. It is collected during summer and autumn. Tripterygium wilfordii Hook is a deciduous climbing vine growing to 12 meters, with brown, angular, downy twigs. The leaves are light green, smooth on top, and pale gray with light hairs underneath.  They have crenate margins and pointed apexes, and are ovate to elliptic, 5-15 cm long, 2.5 - 7 cm wide. The scented hermaphroditic (having male and female organs) flowers, which bloom in September, are small and whitish with five petals and are about 9 mm across, in terminal panicles in July. The fruit is 3-winged, and brownish red, about 1.5 cm long. The plant can grow in light (sandy), medium (loamy) and heavy (clay) soils. It can survive in acid, neutral and basic (alkaline) soil.  It can grow in semi-shade (light woodland) or no shade. It requires moist soil.

Source: The whole plant of Triptergium wilfordil Hook. f., family Celastraceae.



PG490-88 (14-succinyl triptolide sodium salt) is a semisynthetic compound derived from the diterpene triepoxide, triptolide (PG490). PG490 was first isolated and structurally characterized in 1972 when it was extracted from the Chinese medicinal herb, Tripterygium wilfordii Hook F (TWHF), a member of the Celastraceae family. Historically, extracts of TWHF have been used for centuries in traditional Chinese medicine but in the 1970s, they were identified as being effective in the treatment of inflammatory/autoimmune disorders such as rheumatoid arthritis. Since then, more rigorous attempts were made to better identify biologically active constituents of TWHF responsible for its various clinical properties. We now know, for example, that diterpenoid components of TWHF, especially PG490, exert their anti-inflammatory and immunosuppressant effects by inhibition of cytokine production (e.g. , IL-2, IL-4, IFN) by T lymphocytes. These effects of PG490 have also been explored in mouse models where it was shown that PG490 prevents graft versus host disease (GVHD) and prolongs skin, heart, and kidney allograft survival.

The isolation of PG490 has also led to studies supporting its potential development as an antineoplastic agent. Shamon et al., for example, showed that PG490 inhibited growth of several human cancer-derived cell lines (including breast, prostate, and lung) grown in culture. PG490 was also shown to induce apoptosis of human promyelocytic leukemia, T-cell lymphoma, and hepatocellular carcinoma cell lines grown in culture. Interestingly, the inhibitory effects of PG490 on the growth of tumor cells in culture were enhanced in the presence of other inducers of apoptosis such as tumor necrosis factor- (TNF) and chemotherapeutic agents. When combined with chemotherapeutic drugs, PG490 enhanced apoptosis through signaling pathways involving both p53 and p21.

Data on the effects of PG490 on tumor cell growth in vivo , however, are limited. Previous reports have shown that PG490 inhibits tumor development in a hamster model of cholangiocarcinoma and in a murine breast cancer model. These beneficial effects of PG490, however, were counterbalanced by toxicity that was observed at high doses. In the present studies, we further examined the role of PG490 in inhibition of tumor cell growth both in vitro and in a tumor xenograft model. We show that PG490-88, a water-soluble prodrug of PG490, suppresses tumor cell growth in vivo without toxicity. We also show that PG490 acts in synergy with chemotherapy. Our results suggest a potential role of PG490-88 alone and in combination with chemotherapy as a novel antineoplastic regimen for the treatment of patients with solid tumors.

The molecular target(s) for PG490 is currently unknown. Clues to the cellular target, however, are emerging from its effect on transcriptional activity. For example, we have shown along with Qiu et al. , that PG490 blocks transcriptional activation of NF- B by blocking transcriptional activation of p65 but without affecting DNA binding by p65. Additionally, we have found that PG490 blocks transcriptional activation by AP-1 and p53 without affecting DNA binding by Jun/Fos or p53. Recent studies show that the transcriptional activity of AP-1, NF-B, and p53 is regulated by a chromatin structure that is controlled, in part, by histone acetylation. In support of this, a recent study showed that p65 interacts with the histone deacetylase (HDAC) corepressors HDAC1 and HDAC2 to negatively regulate NF- B transcriptional activity. Also, silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) was shown to inhibit transactivation of AP-1, NF-B, and serum response factor (SRF) by binding to their cognate transcription factors. Recent studies also show that p53-mediated transcriptional activity is regulated by histone acetylation. However, we have not observed an effect of PG490 on histone acetyltransferase (HAT) activity or histone acetylation.

PG490 at doses of 5–10 ng/ml does not repress basal transcriptional activity mediated by AP-1, NF-B, and p53 but it does block induction of NF-B by TNF and p53 transcriptional activity induced by chemotherapy. Also, PG490 does not affect topoisomerase I or II activity or increase topoisomerase cleavage complexes. Therefore, its synergy with chemotherapy may in large part be due to its inhibition of p21 mediated growth arrest, which activates an apoptotic pathway.

The treatment of solid tumors is evolving to more targeted treatments that may be helped by genetic profiling of tumors and targeting tumor-specific angiogenic and growth factor pathways. Also, several recent studies have shown that disrupting checkpoints in tumors drives tumor cells into apoptosis by abrogating checkpoint arrest. Here we show that PG490-88, a water-soluble derivative of PG490, reduces tumor growth, induces marked regression, or completely eradicates human tumor xenografts. Moreover, PG490-88 is a potent and well-tolerated antitumor agent that acts in synergy with DNA damaging agents and is effective in a clinically relevant dosing schedule. PG490-88 is now in phase I clinical trials for patients with solid tumors. A recent study showing that PG490 inhibits metastasis of solid tumors coupled with our findings that PG490-88 markedly enhances the cytotoxicity of DNA damaging agents suggests that PG490 or PG490-88 alone or in combination with chemotherapy may become an effective therapy for patients with solid tumors. Also, our finding that PG490 sensitizes tumor cells to TNF by blocking NF-B suggests a role for the combination in treating patients with TNF sensitive tumors such as melanoma. Identification of the target of PG490 and its mechanism of action will complement the ongoing clinical trials, and will provide insight into potential mechanisms of toxicity and the design of compounds that may be more selective and more potent.


1. Saponins

(1). Wilforgine, wilforgine-B,wilfordine, wilfornine, wilfortrine, wilfortrine-D, wilforzine, wilformine, wilfordinic acid, hydroxywilfordii acid ,wilfornine , neowilforine.

(2). Celacinnine, celafurine, celabenzine, celallocinnine.

(3). Triptofordinine A-1, A-2,  triptofordin D-1, D-2, E , triptofordin A, B, C-1 C-2 , triptofordin F-1, F-2, F-3, F-4.

2. Diterpene group

(1). Triptolide, tripdiolide, triptonide,tripterolide.

(2.). Triptolidenol, tripnolide, neotriptophenolide, triptophenolide methyl ether , isoneotrip-tophenolide, hypolide methyl ether.

(3). Triptonoterpene, triptonoterpene methyl ether, triptonoterpenol 12-ydroxy-abieta-8, 11, 13 -trien-3-one, 11-hydroxy-14-methoxy-abieta-8, 11-hydroxy-14-methoxy-abieta-8, 11, 13-trien-3-one.

3. Tetra-triterpene group

(1). Wilforlide A, wilforlide B.

(2). Tritotriterpenoid lactone, tretotriterpenic acid A, tritotriterpenic acid B, tritotriterpenic acid C, 3-epikatonic acid, polpunonic acid, triptodihydroxy acid methyl ester, tripterine.

(3). 3,24-dioxofridelan-29-oic acid, salaspermic acid.

4. Wilfornide

5. 1,8-dihydroxy-4-hydroxymethyl anthraquinone

6. Syringareisno

7 Other Chemicals: dulcitol, glucose, tannin.

8. Trace mineral: iron, manganese, zinc, copper, selenium etc. (source)

中药化学成分 :

从根中分离出生物碱类:雷公藤碱 (tripterygine) 、雷公藤定碱 (wilfordine) 、雷公藤精碱 (wilforgine) 、雷公藤灵碱 (wilforine) 、雷公藤春碱 (wilfortrine) 、雷公藤辛碱 (wilforzine) 、雷公藤酸 (wilfordic acid) 、羟基雷公藤酸 (hydroxy wilfordic acid) 。自石油醚提取物中分离出雷公藤红( tripterin 或 celustrol ),并从残渣的醇提取物中分离出卫矛醇(甜醇 dulcitol ),果糖和葡萄糖。近据报道:雷公藤根皮中含雷酚萜 (tri-ptonoterpene) 、雷酚萜甲醚 (triptonoterpene methylether) 、雷醇内酯 (trip-tolidenol) 、 polounonic acid 、雷二羟酸甲酯、雷公藤三萜内酯 A(triototriterpenoidal lactone A) 、雷酚萜、雷酚萜甲醚及雷醇内酯。
近年来又从雷公藤多甙中分离一新单体为雷公藤氯内酯醇 (tripcheorolide) ,另含一种双环氧二萜化合物为雷藤内酯三醇 (triptriolide) 。
雷公藤所含成分复杂,其有效成分为生物碱,而毒性主要是内酯部分:雷藤酮 (triptonide) 、雷藤甲素 (triptolide) 、雷藤乙素 (tripdiolide) 和山海棠素 (hypolide) 、山海棠素甲醚 (hypolide methyl ether) 、雷藤酮内酯 (triptonolide) 、异雷酚新内酯 (isoneotriptophenolide) 及雷藤素 (wilforonide) 。 茎、叶也含雷藤甲素、雷藤乙素、雷藤酮及一种新的二萜化合物雷公藤内酯二醇酮 (tripdioltonide) 。 (source)

  1. Zhang CP, et al., Studies on diterpenoids from leaves of Tripterygium wilfordii. Yao Xue Xue Bao. 1993.
  2. Liu H, et al., Triptolide: a potent inhibitor of NF-kappa B in T-lymphocytes. Acta Pharmacol Sin. 2000 Sep.
  3. Ning L, et al., Cytotoxic biotransformed products from triptonide by Aspergillus niger. Planta Med. 2003 Sep.
  4. Tao X, et al., Effects of Tripterygium wilfordii hook F extracts on induction of cyclooxygenase 2 activity and prostaglandin E2 production. Arthritis Rheum. 1998 Jan.
  5. Shamon LA, et al., Evaluation of the mutagenic, cytotoxic, and antitumor potential of triptolide, a highly oxygenated diterpene isolated from Tripterygium wilfordii. Cancer Lett. 1997 Jan 15.




Interest in exploiting traditional medicines for prevention or treatment of cancer is increasing. Extracts from the herb Tripterygium wilfordii hook F have been used in China for centuries to treat immune-related disorders. Recently it was reported that triptolide, a purified compound from Tripterygium, possessed antitumor properties and induced apoptosis in a variety of malignant cell lines. K562 cells are usually resistant to apoptosis induction, probably because of the expression of bcr-abl, the hybrid gene characteristic of the Philadelphia chromosome t (9;22). Present studies demonstrate that triptolide inhibited K562 cells proliferation and induced apoptosis in a dose and time-dependent manner. The growth-inhibitory IC50 value for triptolide treatment was 40 ng/ml. Characteristic apoptotic features were confirmed by morphology, internucleosomal DNA fragmentation, and Annexin V Staining. Significantly, triptolide-induced apoptosis of K562 cells was associated with a decline in bcr-abl expression levels, at the concentrations of 20 ng/ml, 40 ng/ml and 80 ng/ml, triptolide was able to decrease the expression of bcr-abl down to 50%, 30% and 20% respectively of the basal value after 72 h.

抗肿瘤:雷公藤内酯、雷公藤内酯二醇 0.1mg/kg 给小鼠,对白血病 L1210 、 P388 有抗肿瘤活性;对人鼻咽癌的 ED50 为 10-3 -10-4 μ g/ml 。雷公藤内酯 0.2 、 0.25mg/kg 腹腔注射,对小鼠白血病 L615 有明显的疗效。雷公藤内酯 1 × 10-8mol/L, 可抑制乳癌与胃癌的四个细胞 MCF-7 、 BT-20 、 MKN-45 、 KATO- Ⅲ软琼酯集落形成,抑制率 70% 以上, IC50 为 0.504-1.22 μ g/L 。

对免疫的影响:雷公藤醋酸乙酯提取物 20 、 40mg/kg, 雷公藤总生物碱 20 、 40mg/kg 灌胃,对小鼠溶血素抗体生成有抑制作用,也抑制小鼠脾细胞溶血空斑形成。雷公藤内酯 75 、 150 μ g/kg 皮下注射可使小鼠血清补体增加,但显著抑制特异性 IgM 抗体形成, 200 μ g/kg 灌胃,抑制小鼠碳粒廓清及腹腔巨噬细胞的吞噬活性,对 2,4- 二硝基氯苯( DNCB )引起的迟发型超敏反应无明显影响。雷公藤红素于试管内 0.1-1.0 μ g/ml, 可以明显抑制 ConA 、 PHA 、 PHM 及 LPS 诱导的脾淋巴细胞增生反应,对淋巴结细胞增生也有相似的抑制作用。雷公藤红素 1mg/kg 腹腔注射,使小鼠血清溶血素抗体生成明显下降;雷公藤红素、雷公藤内酯 0.1-1.0 μ g/ml 显著抑制 ConA 诱导的小鼠淋巴细胞增生,总生物碱 1.0 μ g/ml 也有明显抑制作用;雷公藤红素 10 μ g/ml ,可以明显抑制白细胞的移动。雷公藤总甙 80mg/kg 、总萜 211mg/kg 灌胃,可使小鼠血液白细胞数减少,淋巴细胞总数也减少,嗜中性白细胞与单核细胞相对增加,说明选择性作用于淋巴细胞;脾、胸腺、颌下淋巴结非特异性酯酶 (ANAE) 染色,证明雷公藤总甙、总萜主要作用于 B 细胞而抑制体液免疫。雷公藤春碱、雷公藤新碱 40 、 80mg/kg 腹腔注射,连续 4 天,对经溶血素反应为指标的体液免疫具有抑制作用;雷公藤春碱 160mg/kg 腹腔注射,对小鼠移植物抗宿主反应为指标的细胞免疫也抑制,雷公藤新碱 80mg/kg 腹腔注射,对 2,4- 二硝基氯苯( DNCB )所致迟发型超敏反应具有抑制作用,并能降低小鼠碳粒廓清速率,使小鼠胸腺、脾重减轻。

  1. Yang S, et al., Triptolide inhibits the growth and metastasis of solid tumors. Mol Cancer Ther. 2003 Jan.



Triptolide, from traditional Chinese medicine "Tripterygium wilfordii Hook", has been reported to be effective in the treatment of auto-immune diseases, and it can also induce anti-neoplastic activity on several human tumor cell lines. Studies investigate the cytotoxic function and the functional mechanism of triptolide on tumor cells. Promyelocytic leukemia, (HL-60), T cell lymphoma (Jurkat), and human hepatocelluar carcinoma (SMMC-7721) cells were subjected to triptolide treatment, and cell growth inhibition was examined by XTT cell viability assay. Cell death mechanism (apoptosis) was confirmed through DNA fragmentation and DAPI staining. Triptolide inhibited 50% of cell growth (IC(50)) on HL-60 cells at 7.5 nM, Jurkat cells at 27.5 nM and SMMC cells at 32 nM. Characteristic apoptotic features including internucleosomal DNA fragmentation and chromatin condensation were observed in triptolide treated cells. Data from the study indicates that triptolide could induce apoptosis in human tumor cell lines and it may be applicable as a potential chemotherapeutic agent for cancer treatment.

  1. Lou YJ, Jin J. Triptolide down-regulates bcr-abl expression and induces apoptosis in chronic myelogenous leukemia cells . Leuk Lymphoma. 2004 Feb.
  2. Yang S, et al., Triptolide inhibits the growth and metastasis of solid tumors. Mol Cancer Ther. 2003 Jan.
  3. Jiang Xh, et al., Functional p53 is required for triptolide-induced apotosis a AP-1 and nuclear factor-kappaB activation in gastric cancer cells . Oncogene. 2001 Nov 29.
  4. Tao X, et al., Effects of Tripterygium wilfordii hook F extracts on induction of cyclooxygenase 2 activity and prostaglandin E2 production. Arthritis Rheum. 1998 Jan.
  5. Ujita K, et al., Inhibitory effects of triptogelin A-1 on 12-0-tetradecanoylphorbol-13-acetate-induced skin tumor promotion. Cancer Lett. 1993 Feb.
  6. Zhang CP, et al., Studies on diterpenoids from leaves of Tripterygium wilfordii . Yao Xue Xue Bao. 1993.
  7. Takaishi Y, et al., Inhibitory effects of dihydroagarofuran sesquiterpenes on Epstein-Barr virus activation. Cancer Lett. 1992 July 31.
  8. Wei YS, et al., Inhibitory effect of triptolide on colony formation of breast and stomach cancer cell lines . Zhongguo Yao Li Xue Bao, 1991 Sept.
  9. Shamon LA, et al., Evaluation of the mutagenic, cytotoxic, and antitumor potential of triptolide, a highly oxygenated diterpene isolated from Tripterygium wilfordii. Cancer Lett. 1997 Jan.
  10. Chan EW, et al., Triptolide induced cytotoxic effects on human promyelocytic leukemia, T cell lymphoma and human hepatocellular carcinoma cell lines. Toxicol Lett. 2001 May 31.
  11. Zhou YX, et al., [Several monomes from Tripterygium wilfordii inhibit proliferation of glioma cells in vitro]. Ai Zheng. 2002 Oct.
  12. Panichakul T, et al., Synergistic cytotoxicity and apoptosis induced in human cholangiocarcinoma cell lines by a combined treatment with tumor necrosis factor-alpha (TNF-alpha) and triptolide. Asian Pac J Allergy Immunol. 2002 Sep.
  13. Lee KY, et al., Triptolide sensitizes lung cancer cells to TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inhibition of NF-kappaB activation. Exp Mol Med. 2002 Dec 31.
  14. Liu SX, et al., Molecular analysis of Tripterygium hypoglaucum (level) Hutch-induced mutations at the HPRT locus in human promyelocytic leukemia cells by multiplex polymerase chain reaction. Mutagenesis. 2003 Jan.
  15. Kiviharju TM, et al., Antiproliferative and proapoptotic activities of triptolide (PG490), a natural product entering clinical trials, on primary cultures of human prostatic epithelial cells. Clin Cancer Res. 2002 Aug.
  16. Chang WT, et al., Triptolide and chemotherapy cooperate in tumor cell apoptosis. A role for the p53 pathway. J Biol Chem. 2001 Jan 19.
  17. Ushiro S, et al., New nortriterpenoid isolated from anti-rheumatoid arthritic plant, Tripterygium wilfordii, modulates tumor growth and neovascularization. Int J Cancer. 1997 Aug 7.



Triptolide (PG490), an oxygenated diterpene derived from a Tripterygium wilfordii Hook, induces apoptosis in cultured tumor cells and sensitizes tumor cells to topoisomerase inhibitors by blocking p53-mediated induction of p21. Studies show that PG490-88 is a safe and potent antitumor agent when used alone, causing tumor regression of lung and colon tumor xenografts. It also shows that PG490-88 acts in synergy with CPT-11 to cause tumor regression. A phase I trial of PG490-88 for solid tumors began recently and safety and optimal dosing data should accrue within the next 12 months. The findings that PG490-88 causes tumor regression and that it acts in synergy with DNA-damaging chemotherapeutic agents suggest a role as an antineoplastic agent and chemosensitizer for the treatment of patients with solid tumors.

  1. Chen Y, et al., PG27, an extract of Tripterygium wilfordii hook f, induces antigen-specific tolerance in bone marrow transplantation in mice . Blood 2000 Jan 15.
  2. John M, et al., PG490-88, a devivative of triptolide, causes tumor regression and sensitizes tumors to chemotherapy. Mol Cancer Ther. 2003.
  3. Tengchaisri T, et al., Antitumor activity of triptolide against cholangiocarcinoma growth in vitro and in hamsters. Cancer Lett. 1998 Nov 27.



  1. Kiviharju TM, et al., Antiproliferative and proapoptotic activities of triptolide (PG490), a natural product entering clinical trials, on primary cultures of human prostatic epithelial cells. Clin Cancer Res. 2002 Aug.




1. Toxic reactions: dizziness, palpitation, weakness, nausea, vomiting, stomach ache, diarrhea, pain in liver and kidney areas, bleeding in the digestive tract, even respiration and circulation exhaustion and death.

2. decrease of total blood cell counts.

3. mutation type of illness: using lei gong teng tincture for external use can cause mutation type of illness.

4. Long term use of lei gong teng could significantly decrease bone mineral density of levels in female systemic lupus erythematosus (SLE).

5. long term use of lei gong teng causes hair loss and malfunction of immune system.


I. Prevention

1). For external use: use ointment and avoid tincture.

2). Pay attention to the dosage according to the body constitution of individual patients.

3). Avoid using on patients with liver problems.

II. Antidotes for toxicity.

1). Empty stomach and induce diarrhea.

2). During the early stages, use adrenocortical hormone. Dexamethasone 5~10mg with added 50% glucose 40 ml can be used in IV administering, followed with dexamethasone of 1.5mg, 3 times a day for 2~3 weeks. anisodamine (654-2) can also be used.

3).  Use dextran 40 (low Molecular Dexran, Rheomacrodex) 500ml IV administering, when toxin has been absorbed but no symptom of toxicity. 20% solution of Manitol for IV administering, and furosemide 40mg (Frusemide, Fursemide, Lasix) for muscle injection. Pay attention to the balance of electrolytes and correct acidosis immediately.

4). Skin allergy can be treated with antihistamines or with traditional Chinese herbs for dispersing heat and  neutralizing toxin.

5). Chinese herb treatment:

•  (a) fresh feng wei cao (Pterismultifida Poir) 250 to 500 g each time. Or combine with jin qian cao, wu kuai, tian qi. This single item formula has been successfully used to treat more than 10 serious cases. The combined formula has been used successfully on 7 cases including one who almost died for the toxin. 

•  (b) yang mei (Myrica Zucc) :  drinking juice of the fruit, 100 cc to 200 cc, every 1 or 2 hours, gradually decrease the volume was successful in treating a patient who breathing and heart rate were suddenly stop. Using or bark or root of yang mei 60 to 250 g each time, 2 to 3 times a day is also effective. (Source)

毒性:雷公藤内酯静脉注射对小鼠的 LD50 为 0.8mg/kg ;腹腔注射的 LD50 为 0.9mg/kg 。 20-160 μ g/kg 静脉注射,连续 7 天,使犬血清谷丙转氨酶升高,心电图 T 波异常, ST 段压低, 160 μ g/kg ,使犬体重下降,心肌出现颗粒性变,肝脏灶性坏死,致死原因主要是心、肝的损害。雷公藤总生物碱灌胃小鼠的 LD50 为 1139 ± 204 μ g/kg, 皮下注射为 1136 ± 217 μ g/kg 。雷公藤总生物碱灌胃对小鼠的 LD50 为 504.0 ± 29.48mg/kg 。 (Source)

毒理学: 毒性:雷公藤对各种动物毒性不同,它对人、犬、猪及昆虫的毒性很大,可以发生中毒甚至死亡,但是对羊、兔、猫、鼠、鱼却无毒性。雷公藤对机体的作用有二:一为对胃肠道局部的刺激作用;二为吸收后对中枢神经系统 ( 包括视丘、中脑、延髓、小脑及脊髓 ) 的损害,及引起肝、心的出血与坏死,。有谓雷公藤主要毒害动物的心脏,但对其他平滑肌及横纹肌亦有毒性,此为中毒致死的原因。中毒后急救措施为催吐、洗胃、灌肠、导泻等一般方法,利用羊血或兔胃浸出液的生物学解毒方法尚未确定。雷公藤的毒性成分可用醚浸出,但经过还原作用,毒性完全消失。

中毒与解毒: 1. 雷公藤是一种剧毒药物,尤其皮部毒性极大,使用时应严格剥净皮部,包括二重皮及树缝中的皮分。据有关单位研究,雷公藤对机体的作用有二:一为对胃肠道局部的刺激作用;一为吸收后对中枢神经系统包括视丘、中脑、延脑、小脑及脊髓的损害,并能引起肝、心的出血与坏死。临床所见的一般中毒症状有头晕、心悸、无力、恶心、呕吐、腹痛、腹泻、肝肾区疼痛、血粪等。为慎重起见,对患有心、肝、肾、胃等器质性疾患的病人及孕妇应禁用;对治程中出现恶心呕吐、腹痛腹胀,肝肾区疼痛,尿中出现蛋白及血清转氨酶不正常时,可立即停药。 2. 中毒后一般急救措施:除催吐洗胃、灌肠、导泻外,可服鲜萝卜汁 4 两或炖服莱菔子 8 两,也可用鲜韭菜汗或浓茶、羊血等以解毒。据 20 余个中毒案例的观察,中毒表现均为腹痛、呕吐、腹泻、嚎叫挣扎,但不发热。死亡大都在 24 小时内,最多不超过 4 天。如在服雷公藤后 4 小时内用催吐剂、泻剂,一般均能痊愈. ( Source)

Traditionally, Triptergium wilfordii Hook dispels wind and dampness, and is usually used to treat bi zheng (painful obstruction syndrome). Tripterygium wilfordii Hook relieves pain and reduces swelling in patients who have swollen joints and difficulty moving. It can be used alone or with other antirheumatic herbs.

This herb is also known as qi bu si , literally, "seven steps to death," implying that it is extremely toxic. Because of its toxicity, the daily dose should be kept between five and 12 grams, with a maximum of 15 grams. Classic texts specifically instructed users to peel and discard the root bark of this herb before decocting. In addition, lei gong teng should be cooked for at least 60 minutes before the addition of other herbs, then cooked for another 15 minutes. Prolonged decoction (between one and two hours) is recommended to decrease its toxicity. Side-effects are minimal when this herb is prescribed following the proper dosage and preparation.

Tripterygium wilfordii Hook is contraindicated in pregnancy. It should be used with caution in geriatric and pediatric patients. It should also be used with caution for patients with heart, stomach and spleen disorders. Finally, lei gong teng is toxic, and should not be used by patients who have compromised hepatic functions.