Parkinson’s disease (PD) is a common neurological disorder characterized by dopaminergic (DA) neuron degeneration and death in the midbrain, and the long noncoding RNA HOTAIR has been shown to affect disease progression in PD. In this study, we aimed to further illustrate the molecular mechanism of HOTAIR in PD. Bioinformatics analysis was utilized to determine the potential downstream targets of HOTAIR in PD. Luciferase assay and the RNA Binding Protein Immunoprecipitation (RIP) assay were used to validate the existence of binding sites between competing endogenous RNAs (ceRNAs). Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting indicated that HOTAIR and RAB3IP increased while miR-126-5p decreased in PD cells and PD mice. Additionally, the CCK-8 assay and flow cytometric analysis indicated that the knockdown of HOTAIR and RAB3IP and the overexpression of miR-126-5p significantly increased cell proliferation and reduced apoptosis in PD cells. Furthermore, the results of in vivo experiments suggested that knockdown of HOTAIR expression increased the number of TH-positive cells and the number of α-synuclein-positive cells decreased while reducing the apoptosis rate among DA neurons. Our study confirmed that HOTAIR promotes PD progression by regulating miR-126-5p and RAB3IP in a ceRNA-dependent manner and further clarified how HOTAIR works in PD.

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Increasing evidence verified that oxidative stress and neuroinflammatory response exacerbates motor deficits and increases neuronal loss in several rodent models of Parkinson’s disease. In the present study, we explore the neuroprotective effects of monascin in a rotenone-induced Parkinson’s disease model as well as the underlying mechanisms. Our results showed that monascin remarkedly attenuated behavioral impairments and the depletion of dopaminergic neurons induced by rotenone in the rats. Besides, monascin decreased the levels of pro-inflammatory factors such as interleukin-1β, interleukin-6, tumor necrosis factor-α and oxidative stress marker malondialdehyde while promoted the expression of superoxide dismutase, glutathione peroxidase and other antioxidant factors. Further detection of the expression of related proteins showed that monascin significantly promoted the expression of proliferator-activated receptor-gamma, F-E2-related factor 2 and heme oxygenase-1, but inhibited the expression of NF-κB. What’s more, levels of growth factors that are essential for neuronal and synaptic function were increased under the effects of monascin. All in all, our results revealed that monascin exerted neuroprotective effects in rotenone model of Parkinson’s disease via antioxidation and anti-neuroinflammation.

The aim of this study was to evaluate the diagnostic criteria of dual time point Fluorine-18 fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) in differentiating malignant from benign focal hypermetabolic lesions of duodenum.A total of 50 patients underwent 18F-FDG PET/CT at 2 points: 60 ± 13.7 minutes (early imaging) and 120 ± 26.4 minutes (delayed imaging) after tracer injection. Early maximum standardized uptake value (SUVE), delayed maximum standardized uptake value (SUVD), difference between early and delayed maximum standardized uptake value (D-SUVmax), and retention index (RI) were calculated for each duodenal lesion. Receiver operating characteristic analysis (ROC) was performed to evaluate the discriminating validity of the parameters.There were 32 malignant and 18 benign focal 18F-FDG uptake duodenal lesions. The values of SUVE, SUVD, and D-SUVmax were significantly different between malignant and benign lesions (12.5 ± 6.3 vs 5.8 ± 1.2, 13.5 ± 6.5 vs 5.5 ± 1.1 and 0.3 ± 0.8 vs 1.0 ± 1.0, respectively). The areas under the curves (AUCs) of SUVE, SUVD, D-SUVmax were 0.932, 0.964 and 0.707, respectively. There was no significantly difference between SUVE and SUVD based on AUC. In detecting malignant lesions, SUVE=6.9 yielded a sensitivity of 88.9% and specificity of 84.4%, SUVD=7.2 yielded a sensitivity of 94.6% and specificity of 90.6%, D-SUVmax=0.5 yielded a sensitivity of 72.2% and specificity of 68.8%. SUVD was the best diagnostic indicator, regarding specificity and specificity.SUVE and SUVD had good sensitivity, specificity for differentiating duodenal lesions. But there was no significantly difference between diagnostic value of SUVE and SUVD. 18F-FDG uptake patterns are helpful for differentiating benign and malignant duodenal lesions.