Alzheimer's disease (AD) is associated with the inflammatory response in response to amyloid β-peptide (Aβ). Previous studies have suggested that paeoniflorin (PF) shows anti-inflammatory and neuroprotective effects in inflammation-related diseases. However, the impacts of PF on AD have not been investigated. In the present study, we showed that a 4-week treatment with PF could significantly inhibit Aβ burden, Aβ-induced over activation of astrocytes and microglia, downregulation of proinflammatory cytokines, and upregulation of anti-inflammatory cytokines in the brain. In addition, we demonstrated that chronic treatment with PF inhibited the activation of glycogen synthase kinase 3β (GSK-3β) and reversed neuroinflammtory-induced activation of nuclear factor-kappa B (NF-κB) signaling pathways. Moreover, PF exerted inhibitory effects on NALP3 inflammasome, caspase-1, and IL-1β. Collectively, in the present study, we demonstrated that PF exhibits neuroprotective effects in amyloid precursor protein (APP) and presenilin 1 (PS1) double-transgenic (APP/PS1) mice via inhibiting neuroinflammation mediated by the GSK-3β and NF-κB signaling pathways and nucleotide-binding domain-like receptor protein 3 inflammasome. Thus, these results suggest that PF might be useful to intervene in development or progression of neurodegeneration in AD through its anti-inflammatory and anti-amyloidogenic effects.

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Increasing evidence revealed that the aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in tumorigenesis. However, the role and mechanisms of LINC00662 in glioma have not been elucidated. Here, we show that upregulation of LINC00662 expression in glioma is associated with advanced clinical features and poor prognosis. Our results from loss-of-function assays suggest that LINC00662 silencing suppresses the proliferative and invasive abilities of glioma cells. In vivo, glioma growth was inhibited by depletion of LINC00662 in nude mice. Mechanistically, LINC00662 directly interacts with miR-107. The High-mobility group box 1 protein (HMGB1) is a known target of miR-107. Moreover, rescue assays reveal that HMGB1 overexpression (or miR-107 inhibition) reverses the glioma growth inhibition caused by LINC00662 knockdown. In conclusion, our results indicate that LINC00662 acts as an oncogene in glioma by modulating the miR-107/HMGB1 axis, suggesting that LINC00662 could be a novel therapeutic target for glioma treatment.

ObjectiveNumerous studies have investigated different operative procedures for treating chronic subdural hematoma (CSDH); however, the results are controversial. This meta-analysis was performed to evaluate the efficacy of burr hole drainage without irrigation (BHD) and burr hole drainage with irrigation (BHDI) for CSDH.MethodsWe searched the following electronic databases to identify all studies from their inception to September 2017: Cochrane Library, Science Direct, MEDLINE, EMBASE, Scopus, Google Scholar, the China Biomedical Database (CBM), and the Chinese National Knowledge Infrastructure (CNKI). Randomized clinical trials (RCTs), prospective cohort studies, retrospective observational cohort studies, and case-control studies investigating BHD and BHDI for the treatment of CSDH were included. The Cochrane Collaboration's RevMan 5.3 software was used for meta-analysis.Results:In total, 7 retrospective cohort studies and 2 RCTs involving 993 participants were included. Comprehensive analysis results of 9 studies indicated that the recurrence of the BHDI was similar to that in BHD (odds ratio [OR] = 1.27, 95% confidence interval [CI] = .61–2.63, P = .53). Moreover, analysis for comparing recurrence in the 2 RCTs was not significantly different (OR = 1.14, 95% CI = .16–8.24, P = .95).In addition, meta-analysis of pneumocephalus (OR = 5.91, 95% CI = .61–56.86, P = .12) and mortality (OR = 0.94, 95% CI 0.14–6.16, P = .95) was not significantly different.Conclusions:The results of this meta-analysis demonstrated that procedures with or without irrigation in the treatment of CSDH might have similar effect regarding recurrence and complications; therefore, irrigation might not be necessary. However, well-conducted RCTs and high-quality observational studies are still required to corroborate this issue.