Halofuginone, important discoveries in autoimmune disorders and muscle fibrosi

Published: admin | Format: 2017-02-27

Chang shan(Dichroa febrifuga) is a medicinal herb that has been used for well over 2000 years in traditional Chinese medicine for the treatment of malaria. Its popularity has dwindled as the popular Artemisinin herb has replaced much of its use. However, it has recently been discovered that Chang shan has a selective suppressive effect on the immune system.halofuginone, a compound derived from this extract’s bioactive ingredient, has been the focus of many other studies in the past, too. In a previous one, scientists found that halofuginone could block harmful immune cells from developing, which could be promising in treating autoimmune disorders. some findings also demonstrate the enhancing effect of halofuginone on muscle-cell survival on the one hand, and fibroblast apoptosis on the other, suggesting an additional mechanism for halofuginone's improved effect on histopathology and muscle functions.

1. Halofuginone boost the immune system properties:

"Science" (Sundrud, 2009) magazine reported that a Harvard University on the application of halofuginone for treatment of autoimmune diseases and their mechanism of action. The study found that Chang Shan ketone can specifically inhibit the development of inflammatory cells TH17 and TH17-induced disease, and oral halofuginone also has a role. TH17 cells are derived from the original CD4 + T cells, which were first known in 2006 and are associated with many autoimmune diseases such as rheumatoid arthritis.

The author of the article written by Dr. Mark Sundrud said Halofugenone applied to human autoimmune disease is found in both the first real interference autoimmunity but will not affect the body's immune system to small molecule drugs. The researchers found that the addition of halofuginone in vitro cell systems, TH17 cells is greatly reduced, and from the resulting inflammatory TH17 cells secrete interleukin-17 is also greatly reduced. By autoimmune disease encephalitis model in mice found that the establishment, by adding low doses of halofuginone when TH17 cells can significantly reduce the occurrence of disease have been alleviated. Researchers used microarray gene expression in cells using Halofugenone of the body were tracked and found that halofuginone can "lack of reaction of the amino acid" (amino acid starvation response) pathway activation. At this point we can guess Halofugenone might cause a revolution in the treatment of certain autoimmune diseases and inflammatory diseases.

2. Halofuginone increase muscle function:

Halofuginone also can reduce apoptosis—the presumed cause of satellite-cell depletion during muscle degradation


There are some key points of  additional mechanism by which halofuginone improves muscle pathology and function in muscular dystrophies.

  • Halofuginone treatment reduces the number of apoptotic cells in muscle.

  • Halofuginone decreases muscle-cell apoptosis and increases that of myofibroblasts.

  • Halofuginone's inhibitory effect on muscle-cell apoptosis is PI3K/Akt-mediated.

  • An additional mechanism for halofuginone's improved effects on dystrophic muscle

Anti Muscular Dystrophy & Reduces muscle fibrosis

Setting it well In addition to all the other anti-fibrotic properties, the most important is that halofuginone can cause fibrogenic resolution in animal models and humans. In older fibroblast mdx mice, halofuginone treatment reduced collagen expression levels and improved cardiac and skeletal muscle global function (Huebner, 2008). The ability to elicit pre-existing fibrotic resolution may be mediated by the halofuginone mediating the activity of metalloproteinases (MMPs) derived from (Popov, 2006) and from its effect on the synthesis of matrix inhibitors Metalloproteinases (protease inhibitors) (Bruck, 2001). MMP and their inhibitors in ECM, which play a critical role in the fine regulation of the majority of pathological changes associated with fibrosis.Levi (Levi, 2015) demonstrated an inverse relationship between the level of muscle fibrosis and the level of utrophin and the number of restored muscle fibers. These findings may reveal a common link between fibrosis and the utrophinsynthesis pathway.

Halofuginone reduces muscle fibrosis by inhibiting TGF [beta] signaling and fibroblast-to-myofibroblast transition. (Halevy, 2013) It reduces inflammation by reducing macrophage infiltration into malnourished muscles. (Pines, 2011) Halofuginone promotes myotube fusion and satellite cell survival (Kharraz, 2011). All of these halofuginone effects reduce the number of injured muscle fibers and, together with an increase in the number of utrophin levels and revertants, they lead to an increase in muscle function.


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