Intracerebral hemorrhage (ICH) is a common neurological condition that causes severe disability and even death. Even though the mechanism is not clear, increasing evidence shows the efficacy of atorvastatin on treating ICH. In this study, we examined the impact of atorvastatin on the NOD-like receptor protein 3 (NLRP3) inflammasome and inflammatory pathways following ICH. Mouse models of ICH were established by collagenase injection in adult C57BL/6 mice. IHC mice received atorvastatin treatment 2 h after hematoma establishment. First, the changes of glial cells and neurons in the brains of ICH patients and mice were detected by immunohistochemistry and western blotting. Second, the molecular mechanisms underlying the microglial activation and neuronal loss were evaluated after the application of atorvastatin. Finally, the behavioral deficits of ICH mice without or with the treatment of atorvastatin were determined by neurological defect scores. The results demonstrated that atorvastatin significantly deactivated glial cells by reducing the expression of glial fibrillary acidic protein (GFAP), Ionized calcium binding adapter molecule 1 (Iba1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in ICH model mice. For inflammasomes, atorvastatin also showed its efficacy by decreasing the expression of NLRP3, cleaved caspase-1, and IL-1β in ICH mice. Moreover, atorvastatin markedly inhibited the upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), which indicated deactivation of NLRP3 inflammasomes. By inhibiting the activities of inflammasomes in glial cells, neuronal loss was partially prevented by suppressing the apoptosis in the brains of ICH mice, protecting them from neurological defects.

We carried out the current meta-analysis of relevant cohort studies in an attempt to investigate the relationships between vascular endothelial growth factor (VEGF) expression and pathological characteristics of diffuse large B cell lymphoma (DLBCL). The following electronic databases were searched for relevant articles without any language restrictions: Web of Science (1945 ~ 2013), the Cochrane Library Database (Issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and the Chinese Biomedical Database (CBM) (1982 ~ 2013). Meta-analyses were conducted with the use of STATA software (version 12.0, Stata Corporation, College Station, TX, USA). Odds ratios (ORs) and its 95 % confidence interval (95 % CI) were calculated. Nine clinical cohort studies with a total of 789 DLBCL patients met our inclusion criteria. The meta-analysis results showed that patients with positive VEGF expression had higher international prognostic index (IPI) scores than VEGF-negative patients (OR = 5.12, 95 % CI = 2.70 ~ 9.71, P < 0.001). There was a significantly positive association between positive VEGF expression and evaluated lactate dehydrogenase (LDH) levels (OR = 2.50, 95 % CI = 1.36 ~ 4.60, P = 0.003). We also found that patients with positive B symptoms had increased level of VEGF expression (OR = 2.02, 95 % CI = 1.08 ~ 3.77, P = 0.027). The findings of our meta-analysis provide reliable evidence that VEGF expression may be strongly correlated with pathological characteristics of DLBCL.

Background: Adenoid cystic carcinoma (ACC) is a common tumor of the head and neck. It is characterized by slow growth, strong invasiveness, easy recurrence and distant organ metastasis. Bcl-2 and NF-κB are indicated to relate to tumor growth, proliferation and apoptosis. This study aims to analyze the relationship between Bcl-2, NF-κB and ACC. Methods: With ELISA method to detect Bcl-2 and NF-κB expression in the blood of patients with ACC, patients with benign adenoma and healthy controls, and the expression of Bcl-2 and NF-κB in tissues was detected by immunohistochemistry, and their relationship with ACC was analyzed. relevance. Relationships between clinicopathological features. Results: The levels of Bcl-2 (4.16±1.34 ng/ml) and NF-κB (4.47 ± 1.37 ng/ml) as well as positive rates of Bcl-2 and NF-κB (87.5% and 85%) were significantly elevated in the ACC group (P <0.05). Bcl-2 was positively correlated with NF-κB (P <0.05). Of note, Bcl-2 and NF-κB expressions were correlated with the incidence frequency, histological type, clinical stage, lymph node metastasis and distant metastasis of ACC patients (P < 0.05) as the distant metastasis is an independent risk factor. Conclusion: In summary, Bcl-2 and NF-κB expression in ACC patients is associated with the clinicopathological features of ACC.