ABSTRACT
OBJECTIVE: To analyze the involvement of PI3K/AKT/mTOR signaling pathway on the inhibiting the proliferation of ovarian cancer SKOV3 cell line by olaparib. METHODS: The SKOV3 cells were randomly divided into five groups: control group, olaparib low dose group (10 mg•L-1), olaparib medium dose group (30 mg•L-1), olaparib high dose group (90 mg•L-1), and PI3K protein inhibitor LY294002 group (10 mg•L-1). In addition to the control group, the rest of the cells were incubated with the corresponding doses of the compounds. DAPI and Western blotting were used to analyze the expression of apoptotic protein. qPCR, Western blotting and immunocytochemistry were adopted to detect the expression of PI3K/AKT/mTOR signaling pathway related proteins. RESULTS: After olaparib treatment, the proliferation of ovarian cancer SKOV3 cells was significantly inhibited (P<0.05). Apoptotic bodies in SKOV3 cells increased gradually, and the expression of caspase 3 and caspase 9 increased gradually (P<0.05), PI3K, AKT and mTOR expression gradually decreased (P<0.05) after olaparib medication. With the increase of olaparib level, the above effects were more obvious (P<0.05). CONCLUSION: Olaparib has an inhibitory effect on ovarian cancer SKOV3 cells, and it may play a role by inhibiting the PI3K/AKT/mTOR signaling pathway.
ABSTRACT
OBJECTIVE: To explore the effect of amarogentin on the induction of liver cancer cell line Huh-7 apoptosis and the regulation of PKA/C. METHODS: Liver cancer cell line Huh-7 were divided into 4 groups, control, amarogentin, amarogentin+H89 and amarogentin+H7 group (n=8). The cells were treated with amarogentin (30 mmolL-1) for 6 h besides control group. The amarogentin+H89 and amarogentin+H7 group cells were treated with corresponding compounds at the last 3 h (H89 at 10 mmolL-1 and H7 10 mmolL-1). The apoptotic proteins and MEK/ERK signaling pathway related proteins were detected by Western blotting. The Caspase 3 and Caspase 9 were also be assayed by immune-cytochemistry. At the meaning time, the apoptosis state was assayed by DAPI. RESULTS: The results showed that the Bax, Caspase 3 and Caspase 9 were increased (P>0.05) while the Bcl2 were decreased (P>0.05) expressed greatly after the medication of amarogentin when compared with control. At the same time, the expression of Ras, Rsf, MEK and ERK1/2 were increased (P>0.05) greatly after the medication of amarogentin when compared with control. Those abnormalities were normalized greatly by the medication of H89 (P>0.05) but not H7(P>0.05). CONCLUSION: Amarogentin could promote the apoptosis of liver cancer cell line Huh-7 which is mediated by PKA.
ABSTRACT
Objective To evaluate the efficacy of bivalirudin on reperfusion of coronary artery in patients with acute myocardial infarction undergoing percutaneous coronary intervention. Methods In our study, we evaluated 245 patients with acute myocardial infarction who underwent percutaneous coronary intervention between April 2012 to May 2015. Based on the therapy during operation, bivalirudin were used in 122 patients and heparin was used in 123 patients. Study outcomes included immediate TIMI(thrombolysis in myocardial infarction)flow and CTFC(Corrected TIMI Frame Count)by angiogrophy once the target lesion was opened rates of ,in-hospital thrombocytopenia, bleeding events myocardial infarction, repeat revascularization and the incidence of MACE(major adverse cardiac events)in 30 days and 1 year. Results The mean heart rate was higher in the bivalirudin group(P=0.034). There was no significant difference between the two groups in laboratory results or interventional data(P>0.05). After the target vessel was opened, the effect of bivalirudin on slow/no-reflow in primary PCI has no difference between heparin in terms of TIMI blood evaluation or CTFC (P>0.05). Hospitalization data analysis showed that bivalirudin was able to obtain a higher activated whole blood coagulation time(ACT)value(P<0.001)with lower decrease in the number of platelets. Follow-up data of 30 days and 1 year showed no difference in the incidence of MACE and net adverse clinical events(NACE)between the two groups(P>0.05). Conclusions Bivalirudin has well efficacy and safety in patients with acute myocardial infarction in patients with acute myocardial infarction undergoing PPCI without increasing the incidence of slow/no-reflow.