Study On Antitumor Effect And Mechanism Of Emodin Derivative HXX-37

Object To observe the proliferation and apoptosis related proteins and cells in vitro of tumor cells treated with emodin derivative HXX-37 Effects of ROS content and related protein levels.Discuss whether ROS is involved in HXX-37 to induce apoptosis.Methods1 The antitumor activity of emodin and emodin on Wall cells was detected by Luodan B(Sulforhodamine B,SRB)colorimetry.2 The antitumor activity of emodin and emodin derivatives on the suspension cell jurkat was detected by trimethylazolidazole salt(MTT).3 The ROS levels in tumor cells with different concentration of emodin derivative HXX-37 and different concentration time were detected by ROS kit.5 The ROS levels in tumor cells were meas?red by ROS kit after action of emodin derivative HXX-37.4 Protein extracted from Hep G2 cells was ?sed to detect the effects of xanthin derivative HXX-37 on expression levels of apoptosis-related proteins Bax,Bcl-2,PI3 K,Akt,m TOR,P70S6 K,Caspase 3,Caspase 9.Results 1 The results of Sulforhodamine B showed that the antiproliferative effect of emodin derivative HXX-37 on the tumor cell line(Hep G2,A549)was most significant,and emodin had obvious antiproliferative effect on the above cells.The effect of emodin derivative Hx-37 on the proliferation inhibition of Hep G2 and A549 was obvio?s,and it was dose-and time-dependent.2 Compared with IC50,which acts on Hep G2,emodin acts on 293 cells less than on Hep G2,while HXX-37 acts on 293 cells twice as m?ch as IC50.3 The ROS test showed that the content of ROS in Hep G2 cells and jurkat cells increased significantly after the action of emodin derivative Hx-37,and the content of ROS increased with the action of 1 H,3 H,6 H and 12 H.The final concentration of HXX-37 was 0.8,0.4,0.2 and 0.1 ?mol/L,respectively.After 3 ho?rs,the active oxygen concentration increased significantly with the increase of the concentration,and was concentration and time dependent within a certain dose range.4 Flow cytometry showed that emodin derivative Hx-37 co?ld induce Hep G2 and Jurkat apoptosis,while the death rate of Hep G2 induced by 0.4 ?mol/L HXX-37 was 28.61 %,and the death rate of 0.4?molol / LHx-37 induced Jurkat cell was 50.5 %.Indicates a dose-dependent.5 The results showed that Hep G2 cells were treated with HXX-37,PI3 K,Akt,m TOR,P70S6 K,Bcl-2,Bax,Caspase 3,Caspase 9,and their concentration was increased.Conclusion 1 HXX-37 is more significant than emodin inhibiting tumor proliferation.2 The apoptosis induced by HXX-37 was time-and concentration-dependent.3 Emodin seasonal phosphorus salt derivative HXX-37 can increase the level of ROS in cells,ROS plays an important role in apoptosis induced by emodin derivative.4 The mechanisms by which HXX-37,a 4-emodin derivative,induces Hep G2 apoptosis may be associated with reduced expression of PI3 K,Akt,m TOR,P70S6 K,Bcl-2 protein,thereby activating casasase9 and eventually downstream casasase3.