Anemarrhena Sarsasapogenin Separation And Purification And In Vitro Induced Apoptosis Of Hepg2 Cells

In this research, we isolated sarsasapogenin from Anemarrhena asphodeloides Bunge and studied its potential biological activity, especially its anti-tumor effects.The Anemarrhena asphodeloides Bunge is a kind of in common use Chinese herbal medicine. The sarsasapogenin is a kind of mainly effective components of Anemarrhena asphodeloides Bunge. It has the effect to counteract poison, prevent thirst and lower the blood sugar level. It also shows a role in various physiology functions such as anti-virus infection, anti-platelets aggregation, clearance of free radicals and so on. It can be used to eliminate the thirst in the vexed heat, hot sexually transmitted disease induced high fever, the tuberculosis induced cough and diabetes. It also shows a potential ability to treat with Alzheimers disease and other neuron regeneration diseases. Therefore, the sarsasapogenin has an extensive application possibility in the clinical medicine. However, there are a few reports focused on the anti-tumor effects of sarsasapogenin.The first part of the experiment is the isolation and characterization of sarsasapogenin from Anemarrhena asphodeloides Bunge. We extracted sarsasapogenin from Anemarrhena asphodeloides Bunge by resin, acid-degradation analysis and re-crystallization methods. Then we analyzed the chemical structure and purity of sarsasapogenin by Infrared Spectrum, Mass Spectrometry, NMR and High Performance Liquid Chromatography. The second part of this experiment is the study of the apoptotic effects of sarsasapogenin on human hepatoma HepG2 cells. We treated HepG2 cells by the isolated sarsasapogenin and demonstrated the apoptotic effects of sarsasapogenin by electrophoresis, MTT, flow cytometer, flourrence staining and electronic microscopy.This character of this method includes fast isolation, low cost, high purity and so on. The biological studies showed that the sarsasapogenin can inhibit the HepG2 cells to proliferate obviously, induce the apoptosis of HepG2 cells, and the rate of apoptosis was dose and time dependent.