Introduction: Despite surgical and chemotherapeutical treatment options, the prognosis for glioblastoma (GBM) remains poor. Some studies have found that using lomustine plus bevacizumab to treat GBM can prolong overall survival (OS) and progression-free survival (PFS). The aim of this study was to explore the efficacy of the two drugs in combination treatment of GBM using a meta-analysis of the existing literature to help settle the ongoing debate.Materials and Methods: PubMed, EMBASE, and the Cochrane Library were searched for the effectiveness of lomustine plus bevacizumab in GBM literature, updated on June 6, 2020. The main outcomes analyzed included PFS and OS; the effects of this drug combination on the 6-month PFS, which represents the percentage of patients who had PFS for 6 months, were also analyzed. All the data were pooled: OS and PFS with the mean difference (MD) and 6-month PFS with the risk ratio (RR). Because there were different control groups and dose groups, two subgroup analyses were run to ensure they were comparable. All statistical analyses were performed using the Review Manager Version 5.3 software.Results: Six clinical trials were identified which included 1,095 patients (treatment group: 516; control group: 579). The group treated with lomustine and bevacizumab showed an improvement in OS (MD =1.37; 95% CI, 0.49–2.25; p = 0.002), PFS (MD = 0.23; 95% CI, 0.13–0.34; p < 0.00001), and 6-month PFS (RR = 2.29; 95% CI, 1.43–3.65; p = 0.0005). Two subgroup analyses of the main outcome, OS, show that the results of Control group A (p = 0.01) and Dose group 2 (p = 0.003) are significantly different from those of the other control or dose groups.Conclusion: This study shows that lomustine and bevacizumab can effectively increase OS, PFS, and 6-month PFS in patients with GBM. The encouraging results of the lomustine and bevacizumab combination therapy for GBM should be studied in more clinical trials in the future.

Background/Aim Apoptosis and oxidative stress have been considered as key events in the pathogenesis of Alzheimer’s disease (AD). Senegenin (Sen), the major and most effective ingredient of Radix Polygalae , which has anti-apoptotic and anti-oxidative effects. The aim of this study was to investigate the anti-apoptotic and anti-oxidant effects of Sen on Aβ 1-42 -induced PC12 cells apoptosis and oxidative stress as well as its possible signaling pathway. Methods Rat pheochromocytoma (PC12) cells were treated by 20 μM Aβ 1-42 and then divided into 5 different treatment groups (Control; Aβ 1-42 20 μM; Aβ 1-42 20 μM + Sen 10 μM; Aβ 1-42 20 μM + Sen 30 μM; Aβ 1-42 20μM + Sen 60 μM). PC12 cells activity was detected by MTT assay. Colony formation assay was performed to assess the clonogenic ability of cells. The cell apoptosis was detected by Annexin-V/PI staining. The pro-apoptotic protein (Bax), anti-apoptotic protein (Bcl-2), anti-oxidative stress factor (HO-1, Nuclear Nrf2, Total Nrf2) and pathway-related protein (Akt, P-Akt, PI3K, P-PI3K) were tested by Western blot. The reactive oxygen species (ROS) level was assessed with a DCFH-DA probe. Results The results indicated that Sen dose-dependently increased cell viability and reduced the number of apoptotic cells. The ratio of P-PI3K/PI3K and P-Akt/Akt increased in a dose-dependent manner under the treatment of Sen, suggesting that Sen might activate the PI3K/Akt signaling pathway. Moreover, Sen upregulates the ratio of Bcl-2/Bax. Further study revealed that Sen can play an antioxidant role in enhancing HO-1, promoting Nrf2 nuclear translocation and reducing ROS accumulation to reduce oxidative stress. Conclusion Sen is effective in inhibiting apoptosis and oxidative stress in Aβ 1-42 -induced PC12 cells, which likely contribute to the development of novel therapies for AD.