ABSTRACT
Background: This study aimed to compare the therapeutic efficacy and the side effects of different endostar administration methods in patients with advanced malignancy who underwent second-line chemotherapy. Methods: 98 patients with advanced malignancies were divided into 2 groups based on the delivery methods of endostar, including drip intravenous administration of endostar (DE) group and continuous intravenous administration of endostar (CE) group. Response rate (RR), disease control rate (DCR), and quality of life (QOL) of the patients were examined to evaluate the therapeutic efficacy, and toxicity reactions were analyzed to evaluate the adverse effects. Results: Compared with the DE group, the therapeutic efficacy of CE has been slightly improved, but the difference did not reach statistical significance (P > 0.05). Additionally, no different incidence rate was observed in toxic reactions, including leukopenia, thrombocytopenia, nausea and vomiting, diarrhea, and hepatic function damage, between the DE and CE groups (P > 0.05). Conclusion: In conclusion, no significant difference was observed between the traditional intravenous drip of endostar group and the intravenous drip followed by continuous pumping of endostar group in the patients with advanced malignancies.
ABSTRACT
@#[Abstract] Objective: To observe the effects of shikonin on the proliferation, apoptosis and cell cycle of human esophageal carcinoma TE-1 cells, and to explore its mechanism. Methods: TE-1 cells were treated with different concentrations of shikonin (0, 1, 5, 10 µmol/L). MTT assay was used to detect cell proliferation at different time points (24, 48 and 72 h). After treatment with shikonin for 48 h, cell apoptosis in TE-1 cells of each group was observed with Hoechst 33258 fluorescence staining. Flow cytometry was used to detect apoptosis and cell cycle. The changes in expression of TRAP1/Akt/mTOR signaling pathway related proteins were detected by Western blotting. Results: Shikonin inhibited the proliferation of TE-1 cells in a time-dose-dependent manner (P<0.05 or P<0.01). Compared with the control group, shikonin significantly promoted the apoptosis of TE-1 cells (P<0.01), induced the G0/G1 phase block of TE-1 cells (P<0.05 or P<0.01), and reduced the expression levels of TRAP1, p-Akt and p-MTOR (P<0.05 or P<0.01). The above effects were all dose-dependent. Conclusion: Shikonin can significantly inhibit the proliferation of TE-1 cells in vitro, induce G0/G1 phase arrest and promote apoptosis, which may be closely related to the inhibition of TRAP1/Akt/mTOR signaling pathway.