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Astragaloside VI
DC12126  (CAS:84687-45-6)
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Fields of Application :
Astragaloside VI could activate EGFR/ERK signalling pathway to improve wound healing.
CAS Number: 84687-45-6
Purity:

Molecular Weight: 947.11
Molecular Formula: C47H78O19
Quality Control: HPLCNMR LC/MS(Please contact us to get the QC report)
Synonyms:
Chemical Name:
Storage: 2 years -20C Powder, 2 weeks4C in DMSO,6 months-80C in DMSO
Note: Products for research use only, not for human use
Description:
In Vitro Pretreatment with Astragaloside VI (AS-VI) at 1 M increases EGFR activation in HaCaT cells. Astragaloside VI, a major intestinal metabolite of astragalosides, exerts the strongest EGFR activation. In HaCaT cells, the positive control, EGF expectedly results in 1.50.03-fold increase in cell proliferation, compared to the control. Astragaloside VI at the indicated concentrations also significantly promots cell proliferation in both HaCaT and HDF cells[1]. Astragaloside VI promotes neural stem cell proliferation and enhances neurological function recovery in transient cerebral ischemic injury via activating EGFR/MAPK signaling cascades. In Vivo Astragaloside VI improves wound healing, compared to the control. In the simple noninfected wound model, wound healing in mice is accelerated by Astragaloside VI, where in the time required for wound closure is shortened by approximately 2-4 days, compared to that in the control group. Topical treatment with Astragaloside VI reduces the volume of pus produced, compared to the control group. Astragaloside VI treated wounds show an accelerated rate of healing, compared to the control and vaseline groups. By day 22, the Astragaloside VI -treated wounds fully close, whereas the blank and vaseline-treated wounds do not fully close until day 26. Angiogenesis is a crucial step in the formation of granulation tissue and wound healing. Astragaloside VI increases blood vessel formation in both the non-infected and infected wound models. Astragaloside VI could effectively activate EGFR/MAPK signaling cascades, promote NSCs proliferation and neurogenesis in transient cerebral ischemic brains, and improve the repair of neurological functions in post-ischemic stroke rats.
References:
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