Metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) has been implicated in the pathogenesis of Parkinson’s disease (PD). In addition, resveratrol was shown to regulate the expression of MALAT1. Therefore, the objective of this study was to clarify the role of resveratrol in PD. During the study, luciferase assays were conducted to determine the effect of resveratrol on the transcription efficiency of MALAT1 promoter as well as the regulatory relationships among MALAT1, miR‐129, and SNCA. In addition, real‐time PCR, Western blot analysis, MTT and flow cytometry analyses were conducted to investigate the mechanism of resveratrol in PD. Furthermore, a PD mouse model was established to study the role of resveratrol in vivo. It was found that resveratrol increased the number of TH+ cells and the expression of miR‐129, while decreasing the expression of MALAT1 and SNCA. In addition, MALAT1 inhibited the expression of miR‐129, a negative regulator of SNCA, thus increasing the expression of SNCA. A further mechanistic study revealed that resveratrol inhibited MALAT1 expression by blocking the transcription of the MALAT1 promoter. Finally, MPTP treatment could decrease cell proliferation and increase cell apoptosis, while resveratrol could partly offset the effect of MPTP. In summary, the therapeutic effect of resveratrol in the treatment of PD can be attributed to its ability to modulate the MALAT1/miR‐129/SNCA signaling pathway.
BackgroundWe aimed to determine the risk conferred by metabolic syndrome (METS) and diabetes mellitus (DM) to recurrent stroke in patients with minor ischemic stroke or transient ischemic attack from the CHANCE (Clopidogrel in High‐risk patients with Acute Non‐disabling Cerebrovascular Events) trial.Methods and ResultsIn total, 3044 patients were included. Patients were stratified into 4 groups: neither, METS only, DM only, or both. METS was defined using the Chinese Diabetes Society (CDS) and International Diabetes Foundation (IDF) definitions. The primary outcome was new stroke (including ischemic and hemorrhagic) at 90 days. A multivariable Cox regression model was used to assess the relationship of METS and DM status to the risk of recurrent stroke adjusted for potential covariates. Using the CDS criteria of METS, 53.2%, 17.2%, 19.8%, and 9.8% of patients were diagnosed as neither, METS only, DM only, and both, respectively. After 90 days of follow‐up, there were 299 new strokes (293 ischemic, 6 hemorrhagic). Patients with DM only (16.1% versus 6.8%; adjusted hazard ratio 2.50, 95% CI 1.89–3.39) and both (17.1% versus 6.8%; adjusted hazard ratio 2.76, 95% CI 1.98–3.86) had significantly increased rates of recurrent stroke. No interaction effect of antiplatelet therapy by different METS or DM status for the risk of recurrent stroke (P=0.82 for interaction in the fully adjusted model of CDS) was observed. Using the METS (IDF) criteria demonstrated similar results.ConclusionsConcurrent METS and DM was associated with an increased risk of recurrent stroke in patients with minor stroke and transient ischemic attack.
SAP was more closely related with diabetes, age, consciousness, days of hospitalization, tracheal intubation, tracheal incision, nasal feeding treatment, and the application of H₂-receptor blocking agents and antimicrobials.
GM-1 ganglioside (GM-1) has been proposed as a new therapeutic agent against Alzheimer's disease (AD). Therefore, in this study we aimed to investigate the effects of GM1 on memory deficits and oxidative stress in the hippocampus of rat model of AD. Wistar rats were randomly divided into three groups (n = 15): control group, model group, and treatment group, which were injected with vehicle, Aβ1-40, and Aβ1-40 together with GM-1, respectively. Morris water maze test was performed to evaluate spatial learning and memory of the rats. Brain malondialdehyde (MDA) content was detected by biochemical assay, and 4-hydroxynonenal (4-HNE) level in the hippocampus was examined by immunohistochemistry. The results showed that learning and memory deficits were improved in treatment group compared to model group. Brain MDA content and 4-HNE level in hippocampus CA1 were much lower in treatment group than in model group. In summary, we demonstrate that GM-1 could improve spatial learning and memory deficits in rat model of AD, and this may be mediated by the inhibition of oxidative stress and lipid peroxidation in the neurons. These data suggest that GM-1 is a potential agent for AD treatment.
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