It remains controversial as to whether mechanical thrombectomy (MT) is safer and more beneficial in patients with large vessel occlusion stroke (LVOS) presenting with a National Institutes of Health Stroke Scale score ≤ 8. We therefore conducted a meta-analysis of the published data.We searched PubMed and Embase and pooled relevant data in the meta-analyses using fixed effects models. Only studies that directly compared best medical therapy alone (BMT) with MT were included. We used odds ratios to analyze the associations between MT and 90-day functional outcome (evaluated using the modified Rankin Scale (mRS)), mortality, and rates of symptomatic intracerebral hemorrhage (sICH) in patients with LVOS and minor symptoms. Five studies including a total of 581 patients met our inclusion criteria. A significant difference was found that the patients treated with MT were associated with improved 90-day mRS score (OR, 1.68; 95% CI, 1.08–2.61) compared with BMT group. There was no difference in 90-day mortality between the two groups. However, sICH occurred more frequently in the MT group than the BMT group (OR, 3.89; 95% CI, 1.83–8.27). Patients with LVOS with minor or mild symptoms who underwent primary thrombectomy had a significantly improved 90-day mRS score compared to those who received BMT alone. Meanwhile, the risk of sICH was higher in the MT group than that in BMT group. Future randomized clinical controlled trials evaluating the role of endovascular reperfusion for LVOS with minimal symptoms are warranted.

The present study investigated the role of aminoguanidine in the prevention of harmful effects in astroglioma F98 cells induced by β‑amyloid treatment. MTT assay was used to analyze cell viability. Expression of inducible nitric oxide synthase (iNOS) was analyzed using western blot analysis. Treatment of the F98 cells with a 15 µM concentration of β‑amyloid for 12 h reduced cell viability to 18% compared with the control cells. However, pretreatment with a 30 µM concentration of aminoguanidine for 12 h completely prevented the β‑amyloid‑induced reduction in cell viability. The production of ROS and the expression of iNOS were significantly (P<0.005) higher in the β‑amyloid‑treated F98 cells. Aminoguanidine pre‑treatment inhibited the β‑amyloid‑induced increase in the expression of ROS, with increased mRNA and proteins levels of iNOS12 h following treatment at a 30 µM concentration. The β‑amyloid treatment also resulted in a marked increase in the expression of cyclooxygenase‑2 (COX‑2) in F98 cells. By contrast, pre‑treatment with aminoguanidine for 12 h led to reduction in the mRNA and protein expression levels of COX‑2. Pre‑treatment of the F98 cells with aminoguanidine at a 30 µM concentration for 12 h prior to incubation with β‑amyloid significantly (P<0.002) reduced the expression of prostaglandin E2 (PGE2). Aminoguanidine pre‑treatment also caused the inhibition of β‑amyloid‑induced translocation of nuclear factor (NF)‑κB p65 into the cytosol. Thus, aminoguanidine prevented β‑amyloid‑induced Alzheimer's disease through reductions in the expression levels of NO, iNOS, PGE2 and COX‑2, and the inactivation of NF‑κB. Therefore, aminoguanidine offers potential for use in the treatment of neurological disorders, including Alzheimer's disease.