Natural Cancer Treatment in Thunder God Vine Studied in Detroit, Michigan

Cancer – a terrifying diagnosis, a rampant disease and a killer of loved ones world wide.  Cancer knows no mercy, it shows no compassion for our children or our grandparents, our world thought leaders or our beloved neighbor.  And the treatment for cancer, those heralded by the giant pharmaceutical companies and the mainstream medical practitioner is oftentimes as harrowing as the disease itself.

 Thunder God Vine

But it doesn’t have to be.  There are alternatives.

One such alternative cancer treatment is Thunder God Vine.  The studies have been numerous and the results have been very promising – which only validates what practitioners of Chinese medicine have known for centuries.

Thunder god vine (Lei Gong Teng, Thunder Duke Vine, or Tripterygium Wilfordii Hook F) is made of many natural compounds, and two key components are Celastrol and Triptolide, which treat cancer naturally in different ways.  Thunder god vine belongs to a group of plants known as Celastraceae, native to the far east.  The aerial parts of the plant are toxic and can be used as a natural pest control, but the peeled root of the plant holds intense medicinal properties and has been used for centuries by the Chinese to fight cancers, tumors and inflammatory diseases.  Dr. Huanjie Yang at the Barbara Ann Karmanos Cancer Institute in Detroit, Michigan, studies the effects of different Chinese herbs on cancer , and specifically, how different herbs effect the protease complex necessary for the growth of cancer cells.

Cancer cells, according to Dr Yang, require a protease complex in order to grow, as do normal human cells.  However, cancer cells seem more vulnerable to death when protease inhibiting compounds are introduced to the body, causing aptosis (or cell death) of tumor cells much more quickly than normal or non-cancerous cells.

 

Triptolide, one of the primary components of the thunder god root, is a diterpenetriepoxide which inhibits tumor cell growth at low doses and causes tumor cell death at higher doses.

According to Dr. Yang’s study…

  • Triptolide inhibited transactivation of NF-κB induced by Tumor Necrosis Factor-α (TNF-α) and further blocked NF-κB-mediated induction of the inhibitor of apoptosis c- Inhibitor of Apoptosis Protein 1 (IAP1) and c-IAP2.
  • Triptolide inhibited NF-κB transactivation without inhibiting nuclear NF-κB DNA binding activity … or even with increased nuclear NF-κB DNA binding activity.
  • Triptolide inhibited the binding of p65 to transcriptional coactivator CBP/p300.
  • Triptolide also suppressed the phorbolmyristyl acetate (PMA)-induced activation of NF-κB, in turn, inhibited the overexpression of urokinase-type plasminogen activator receptor (uPAR), which is required for tumor cell invasion.
  • In addition, Triptolide inhibited up to 80% mRNA de novo synthesis in various tumor cells by inhibiting RNA polymerase I and II, indicating that it hits a wide spectrum of targets.

 

Celastrol is the secondary compound that was studied by Dr Yang and his team as a derivative of Thunder God Vine.

Celastrol is a quinonemethide triterpene isolated from lei gong teng.  Dr Yang and his team “predicted that celastrol is a proteasome inhibitor by molecular modeling and later confirmed its proteasome-inhibitory activity by in vitro and in vivo experiments” .

Celastrol potently and preferentially inhibits the chymotrypsin-like activity of a purified 20S proteasome with an IC50 value 2.5 μmol/L.  In intact human prostate cancer cells, cellular 26S proteasome was inhibited by celastrol at 1–5 μmol/L. The inhibition of the proteasome activity by celastrol results in accumulation of ubiquitinated proteins and three natural proteasome substrates (IκB-α, Bax and p27), and induction of apoptosis in androgen receptor-positive or androgen receptor-negative prostate cancer cells. Treatment of human prostate tumor-bearing nude mice with celastrol (1–3 mg/kg/day, i.p., for 1 to 31 days) resulted in significant inhibition (65–93%) of the tumor growth. Multiple assays using the animal tumor tissue samples from both early and end time-points demonstrated in vivo inhibition of the proteasomal activity and induction of apoptosis after celastrol treatment. These results demonstrate that celastrol is a natural proteasome inhibitor that has a great potential to be used for cancer prevention and treatment [31].

Celastrol has also been determined to be effective against other types of cancers, such as breast cancer, inhibiting tumor growth effectively by targeting the cysteine 179 in the IκB-α kinase (IKK). Celastrol was able to produce cell death and suppress NF-kB activation, which is a complex in cells that controls the transcription of DNA.  Improper regulation in the body of the NF-kB inhibits the body’s response to infection and inflammation.

According to Dr Yang, Celastrol also…

  • Inhibits Hsp90 by resulting in suppression of its client proteins that play an important role in tumor initiation and progression.
  • Celastrol also suppressed androgen receptor (AR) that mediates signaling important for prostate cancer progression .
  • The aryl hydrocarbon receptor (AhR) is a client protein of Hsp 90, which plays a significant role in polycyclic aromatic hydrocarbon (PAH)-induced carcinogenesis.
  • Celastrol suppressed AhR expression, resulting in decreased transctivation of CYP1A1 and CYP1B1, both of which encode proteins that convert PAH to genotoxic metabolites.
  • Celastrol also inhibited antiangiogenesis by suppressing vascular endothelial growth factor (VEGF) receptors expression.

Does this research mean that Thunder god vine will cure every form of cancer that is out there? No, it does not – but what it does mean is that is can be a viable alternative treatment, and for those who do not want to undergo the chemical warfare that is chemotherapy, this is an alternative treatment method to consider.

References

Yang, Huanjie, Jinbao Liu, and Q. Ping Dou.“Targeting Tumor Proteasome with Traditional Chinese Medicine.” Current Drug Discovery Technologies 7.1 (2010): 46–53. Print.

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