Plant Extracts Triptolide CAS: 38748-32-2 for Anti-Rheumatoid Action

Plant extracts Triptolide CAS: 38748-32-2 for anti-rheumatoid action

Quick detail;

Product Name: triptolide TWH
English name: Triptolide
Detection methods: external standard method
CAS: 38748-32-2
Triptolide Synonyms: triptolide, triptolide, Ray palmatine A
Molecular formula: C20H24O6
Molecular Weight: 360.4
Specifications content: 98% -99%
Heavy metals: <10PPM
Microbiological criteria:
The total bacterial count: <1000CFU / g
Mold and yeast: <100CFU / g
Production process: mainly provided by the alcohol, extraction, chromatography, crystallization processes completed
Storage: cool, dry, dark, avoid high temperature
Triptolide shape: white needle-like crystal
Physical properties: mp 227-228 ºC, insoluble in water, soluble in methanol, ethyl acetate, chloroform and the like.
 
Description;

During kidney organogenesis, tubular epithelial cells proliferate until a functional tubule is formed as sensed by cilia bending in response to fluid flow. This flow-induced ciliary mechanosensation opens the calcium (Ca2+) channel polycystin-2 (PC2), resulting in a calcium flux-mediated cell cycle arrest. Loss or mutation of either PC2 or its regulatory protein polycystin-1 (PC1) results in autosomal dominant polycystic kidney disease (ADPKD), characterized by cyst formation and growth and often leading to renal failure and death. Here we show that triptolide, the active diterpene in the traditional Chinese medicine Lei Gong Teng, induces Ca2+ release by a PC2-dependent mechanism. Furthermore, in a murine model of ADPKD, triptolide arrests cellular proliferation and attenuates overall cyst formation by restoring Ca2+ signaling in these cells. We anticipate that small molecule induction of PC2-dependent calcium release is likely to be a valid therapeutic strategy for ADPKD.

ACTION: triptolide is not only anti-rheumatoid action, has confirmed it has anti-inflammatory, immuno-suppression, anti-senile dementia, and other pharmacological activity, but with a certain toxicity

Application;

This natural product, isolated from the medicinal vine Tripterygium wilfordii Hook F ("Thunder God Vine") and used in traditional Chinese medicine for centuries, has a myriad of therapeutic uses against cancer, inflammation, and autoimmune diseases . Triptolide has been shown to induce apoptosis or cell growth arrest depending on its concentration and the cell type treated . It is also a potent inhibitor of NF-κB- and NF-AT-mediated transcription, and therefore leads to the down-regulation of many gene products necessary for the inflammatory response or cellular growth. We have additionally shown that triptolide's mode of action can be differentiated by a calcium dependence because cell growth and cell death are sensitive to calcium concentrations, but transcriptional inhibition is not . Although studies on triptolide-mediated downstream signaling events have elucidated important biological findings, basic cellular interactions and potential binding proteins have not been identified. Our results here present an as of yet undescribed mechanism of action for triptolide and an ability to stimulate Ca2+ release, arrest cell growth, and reduce cyst progression in a model of ADPKD.

Specification:
  Plant extracts Triptolide CAS: 38748-32-2 for anti-rheumatoid action

Quick detail;

Product Name: triptolide TWH
English name: Triptolide
Detection methods: external standard method
CAS: 38748-32-2
Triptolide Synonyms: triptolide, triptolide, Ray palmatine A
Molecular formula: C20H24O6
Molecular Weight: 360.4
Specifications content: 98% -99%
Heavy metals: <10PPM
Microbiological criteria:
The total bacterial count: <1000CFU / g
Mold and yeast: <100CFU / g
Production process: mainly provided by the alcohol, extraction, chromatography, crystallization processes completed
Storage: cool, dry, dark, avoid high temperature
Triptolide shape: white needle-like crystal
Physical properties: mp 227-228 ºC, insoluble in water, soluble in methanol, ethyl acetate, chloroform and the like.
 
Description;

During kidney organogenesis, tubular epithelial cells proliferate until a functional tubule is formed as sensed by cilia bending in response to fluid flow. This flow-induced ciliary mechanosensation opens the calcium (Ca2+) channel polycystin-2 (PC2), resulting in a calcium flux-mediated cell cycle arrest. Loss or mutation of either PC2 or its regulatory protein polycystin-1 (PC1) results in autosomal dominant polycystic kidney disease (ADPKD), characterized by cyst formation and growth and often leading to renal failure and death. Here we show that triptolide, the active diterpene in the traditional Chinese medicine Lei Gong Teng, induces Ca2+ release by a PC2-dependent mechanism. Furthermore, in a murine model of ADPKD, triptolide arrests cellular proliferation and attenuates overall cyst formation by restoring Ca2+ signaling in these cells. We anticipate that small molecule induction of PC2-dependent calcium release is likely to be a valid therapeutic strategy for ADPKD.

ACTION: triptolide is not only anti-rheumatoid action, has confirmed it has anti-inflammatory, immuno-suppression, anti-senile dementia, and other pharmacological activity, but with a certain toxicity

Application;

This natural product, isolated from the medicinal vine Tripterygium wilfordii Hook F ("Thunder God Vine") and used in traditional Chinese medicine for centuries, has a myriad of therapeutic uses against cancer, inflammation, and autoimmune diseases . Triptolide has been shown to induce apoptosis or cell growth arrest depending on its concentration and the cell type treated . It is also a potent inhibitor of NF-κB- and NF-AT-mediated transcription, and therefore leads to the down-regulation of many gene products necessary for the inflammatory response or cellular growth. We have additionally shown that triptolide's mode of action can be differentiated by a calcium dependence because cell growth and cell death are sensitive to calcium concentrations, but transcriptional inhibition is not . Although studies on triptolide-mediated downstream signaling events have elucidated important biological findings, basic cellular interactions and potential binding proteins have not been identified. Our results here present an as of yet undescribed mechanism of action for triptolide and an ability to stimulate Ca2+ release, arrest cell growth, and reduce cyst progression in a model of ADPKD.

Specification: