[Objective] To observe the inhibiting capacity of Bingcha Shuan Containing serum to HEPG2 cells' reproductive activity and to conjecture.Bingcha Shuan has the potential to cure the liver carcinoma.[Method]According to serum pharmacology,HEPG2 cells were cultured in vitro and interfered by various concentrations of Bingcha Shuan contained serum for 24,48 hours respectively.The inhibiting capacity of the Bingcha Shuan contained Serum to HEPG2 cells were detected by MTT.[Result] The Bingcha Shuan contained Serum has the inhibiting capacity to HEPG2 cells in some degree.And there was a marked positive correlation between drug concentration,time and inhibition ratio.[Conclusion] It is suggested that Bingcha Shuan has the inhibiting capacity of cell proliferation and it can provide the support on how to cure the liver cancer of clinic.

AIM: To study the effects of Bingcha Embolus on the proliferation, apoptosis and cell cycle of astrocytes in vitro in terms of serum pharmacology. METHODS: The cerebral cortex astrocytes of neonatal Sprague-Dawley rats were cultivated in vitro, and the purified astrocytes were randomly devided into Bingcha Embolus groups (high dose, middle dose, low dose) and control group after being identified by means of immunocytochemical method. After the incubation of 48 h with sera, MTT was employed as a proper method to detect the proliferation of astrocytes. The ratio of apoptosis and different cell cycle phases were measured by Flow Cytometry. RESULTS: The results of MTT showed that the cell number of Bingcha Embolus groups (high dose, middle dose) were obviously fewer than that of the control group (P

[Objective]To study the effects of oridonin on Bel-7402/Sora cell proliferation,apoptosis,cycle and phosphatidylinositol 3-kinase/protein kinase B(PI3K/AKT)signaling pathway.[Methods]The concentration gradient increasing method was used to establish Bel-7402/Sora drug-resistant cell line.Cell counting kit-8(CCK-8)method was used to detect cell proliferation inhibition rate and calculate cell resistance reversal index,flow cytometry was used to detect the cell apoptosis and cell cycle,Real-time quantitative polymerase chain reaction(RT-PCR)method was used to detect mRNA expression level of PI3K,AKT and mammalian target of rapamycin(mTOR),Western blot method was used to detect PI3K,AKT,mTOR protein expression levels.[Results]Compared with blank control group,oridonin with final concentrations of 4,8,16,32,64 μmol·L-1 had a better proliferation inhibition on Bel-7402/Sora cells(P<0.05,P<0.01),and the effect was dependent on concentration.The resistance reversal index of oridonin on Bel-7402/Sora cells is 2.024.Compared with blank control group,the early,late and total apoptosis rate of oridonin group were significantly increased(P<0.01,P<0.05);compared with oridonin group,the early and total apoptosis rate of oridonin jointed Sorafenib group were significantly increased(P<0.05).Compared with blank control group,the proportion of G2 phase cells of oridonin group was significantly increased(P<0.01);compared with oridonin group,the proportion of G1 phases cells of oridonin jointed Sorafenib group was significantly increased,and G2 phases cells was significantly decreased(P<0.01).Compared with blank control group,PI3K,AKT and mTOR mRNA expression levels of oridonin group were significantly reduced(P<0.01);compared with oridonin group,PI3K,AKT and mTOR mRNA expression levels of oridonin jointed Sorafenib group were significantly reduced(P<0.01).Compared with blank control group,PI3K and AKT protein expression levels of oridonin group were significantly reduced(P<0.01),and mTOR protein expression levels were no statistical significance(P>0.05);compared with oridonin group,AKT protein expression levels of oridonin jointed Sorafenib group were significantly reduced(P<0.01),PI3K,mTOR protein expression levels were no statistical significance(P>0.05).[Conclusion]Oridonin can inhibit cell proliferation of Bel-7402/Sora cell,induce apoptosis,hinder cycle progression and its anti-tumor mechanism may be related to intervene in the PI3K/AKT signaling pathway.