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Neuroinflammation plays important roles in the pathogenesis and progression of altered neurodevelopment, sensorineural hearing loss, and certain neurodegenerative diseases. Hyperoside (quercetin-3-O-β-D-galactoside) is an active compound isolated from Hypericum plants. In this study, we investigate the protective effect of hyperoside on neuroinflammation and its possible molecular mechanism. Lipopolysaccharide (LPS) and hyperoside were used to treat HT22 cells. The cell viability was measured by MTT assay. The cell apoptosis rate was measured by flow cytometry assay. The mRNA expression levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) were determined by quantitative reverse transcription polymerase chain reaction. The levels of oxidative stress indices superoxide dismutase (SOD), reactive oxygen species (ROS), catalase (CAT), glutathione (GSH), and malondialdehyde (MDA) were measured by the kits. The expression of neurotrophic factor and the relationship among hyperoside, silent mating type information regulation 2 homolog-1 (SIRT1) and Wnt/β-catenin, and sonic hedgehog was examined by western blotting. In the LPS-induced HT22 cells, hyperoside promotes cell survival; alleviates the level of IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax, and caspase-3; and increases the expression of CAT, SOD, GSH, Bcl-2, BDNF, TrkB, and NGF. In addition, hyperoside upregulated the expression of SIRT1. Further mechanistic investigation showed that hyperoside alleviated LPS-induced inflammation, oxidative stress, and apoptosis by upregulating SIRT1 to activate Wnt/β-catenin and sonic hedgehog pathways. Taken together, our data suggested that hyperoside acts as a protector in neuroinflammation.

Malignant glioma is the most common and lethal type of primary tumor of the central nervous system. The incidence of glioma is increasing year by year. In recent years, a variety of new treatment methods have emerged, among which gene therapy has become a hotspot. MicroRNAs (miRNAs) are a class of small non-coding single-strand RNAs that negatively regulate gene expression at the post-transcriptional and/or translational level by binding loosely complimentary sequences in the 3' untranslated regions (UTRs) of target mRNAs. Several miRNAs have been reported to modulate glioma progression. This study aimed to determine the function of miR-30b-5p in glioma and its underlying molecular mechanism. miR-30b-5p expression was significantly lower in gliomas than the normal brain tissues. Overexpression of miR-30b-5p was found to significantly inhibit glioma cell proliferation in vitro. Further, MTDH expression was significantly higher in the gliomas compared with the normal brain tissues. In addition, MTDH was validated as direct target of miR-30b-5p. Moreover, cellular proliferation was increased after MTDH overexpression in the glioma cells, which reversed the effects of miR-30b-5p. Taken together, these results reveal miR-30b-5p impacts glioma cell proliferation via direct targeting MTDH and could be a potential novel therapeutic target for the treatment of glioma.

Glioblastoma multiforme (GBM) is defined by the World Health Organization as the most aggressive form of grade IV glioma, characterized by unrestrained cellular proliferation. microRNAs (miRs) serve important roles in the pathogenesis of GBM. However, the function of miR-194-5p in GBM remains unknown. In the present study, the miR-194-5p levels in GBM tissues and cells were evaluated using the reverse transcription-quantitative polymerase chain reaction. Cellular proliferation was tested by MTT analysis. Cellular apoptosis was analyzed by fluorescence-activated cell sorting. The protein level of insulin-like growth factor 1 receptor, the target gene of miR-194-5p, was evaluated by western blotting. The interaction between miR-194-5p and the target gene was confirmed by the dual-luciferase reporter assay. It was demonstrated that miR-194-5p inhibited cell growth and promoted apoptosis. In conclusion, the results of the present study indicated the tumor suppressive role of miR-194-5p.