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The objective of this study was to explore the protective effects of hydroxy fullerenes (HFs) on cognitive function in rats with temporal lobe epilepsy (TLE) and to elucidate the underlying mechanisms. Eighteen Sprague-Dawley (SD) rats were randomly selected and administered pilocarpine (50 mg/kg) intraperitoneally to establish a TLE model, and were then randomly assigned to the TLE group and the TLE + HFs group. An additional nine SD rats were served as a normal control group (CON group). The Morris water maze (MWM) test was utilized to assess the spatial learning and memory capabilities of the rats. Nissl staining was employed to observe the survival neurons in the CA1 and CA3 regions. In addition, the ultrastructure of synapses in the CA1 region was examined using transmission electron microscopy (TEM). The expressions of postsynaptic densitin-95 (PSD-95) and synaptophysin (SYP) in the hippocampus were detected via western blotting. The findings revealed that compared to the CON group, the TLE group exhibited significantly prolonged escape latency, reduced platform crossing frequency, and shortened time spent in the target quadrant. The number of surviving neurons in the CA1 and CA3 regions and the expression of PSD95 and SYP protein were significantly decreased ( P  < 0.05 or P  < 0.001). However, these alterations were reversed in the TLE + HFs group. It is suggested that HFs may enhance the spatial learning and memory ability of TLE rats by preserving the integrity of hippocampal neurons, up-regulating the expression of SYP and PSD95 in hippocampus.

The aim of this study was to evaluate the neuroprotective effect of tanshinone IIA (TSA) on focal cerebral ischemia in rats and to investigate whether it was associated with Nogo-A/NgR1/RhoA/Rho-associated protein kinase 2 (ROCKII)/myosin light chain (MLC) signaling. In this study, focal cerebral ischemia animal model was used. Neurological deficit scores and infarction volume were investigated to evaluate the neuroprotection of TSA. Hematoxylin-eosin staining, Nissl staining, and immunofluorescence staining were conducted to detect ischemic changes in brain tissue and changes in neurofilament protein 200 (NF200) and growth-associated protein-43 (GAP-43) expression, respectively. Western blotting and qRT-PCR analyses were used to detect the expression levels of NF200, GAP-43 and Nogo-A/NgR1/RhoA/ROCKII/MLC pathway-related signaling molecules. TSA treatment can improve the survival rate of rats, reduce the neurological score and infarct volume, and reduce neuron damage. In addition, TSA also increased axon length and enhanced expression of NF200 and GAP-43. Importantly, TSA significantly attenuated the expression of Nogo-A, NgR1, RhoA, ROCKII, and p-MLC, and thus inhibiting the activation of this signaling pathway. TSA promoted axonal regeneration by inhibiting the Nogo-A/NgR1/RhoA/ROCKII/MLC signaling pathway, thereby exerting neuroprotective effects in cerebral ischemia rats, which provided support for the clinical application of TSA in stroke treatment.

To explore whether miR-199a-5p regulated BBB integrity through PI3K/Akt pathway after ischemia stroke. Adult male Sprague-Dawley rats with permanent middle cerebral artery occlusion(MCAO) were used in experiment. The Ludmila Belayev 12-point scoring was used to measure the neurological function of MCAO rats. The Evans Blue Stain, immunofluorescence staining, western-blotting and RT-PCR were performed to evaluate the effects of miR-199a-5p mimic on BBB integrity in rats following MCAO. The result suggested that miR-199a-5p mimic treatment possessed the potential to boost proprioception and motor activity of MCAO rats. MiR-199a-5p decreased the expression of PIK3R2 after MCAO, activated Akt signaling pathway, and increased the expression of Claudin-5 and VEGF in the ischemic penumbra. Furthermore, miR-199a-5p alleviated inflammation after cerebral ischemia. BBB leakage and neurocyte apoptosis were cut down in MCAO rats treated with miR-199a-5p mimic. MiR-199a-5p mimic decreased the expression of PIK3R2 and activated Akt signaling pathway after ischemia stroke, reduced the expression of inflammatory cytokines, and attenuated BBB disruption after ischemic stroke.

The present study aimed to explore the effect of osmotic stimuli on intervertebral discs (IVDs) using microarray analysis. Gene expression dataset GSE1648 was downloaded from the Gene Expression Omnibus database. There were 11 IVD cell samples in this dataset, which included 4 hyperosmotic stimuli samples, 3 hypoosmotic stimuli samples and 4 isosmotic stimuli samples. The differentially expressed genes (DEGs) in hyperosmotic or hypoosmotic IVD cells (designated DEGs-hyper or DEGs-hypo) were identified, compared with isosmotic cells, using the limma package of R software. The Database for Annotation, Visualization and Integrated Discovery was used to perform a Gene Ontology (GO) term enrichment analysis for the DEG sets. Protein-protein interaction (PPI) network and microRNA (miRNA) gene-regulatory network data for the DEG sets were obtained using the Human Protein Reference Database (HPRD) and the TargetScan database, respectively, and these networks were constructed and visualized using Cytoscape software. There was a total of 43 DEGs in DEGs-hyper and 9 in DEGs-hypo. Analysis of DEGs-hyper revealed that 41 GO terms were significantly enriched. In total, 376 pairs and 382 nodes were involved in the PPI network, and 1,314 miRNA-gene pairs and 422 nodes were contained in the miRNA-gene-regulated network. The results of the present study indicated that potential target genes (including , , , , and ) may be involved in the effect of osmotic stimuli on IVD, and the biological processes of apoptosis and cell death may be associated with the effect of high osmolality on IVD disease. The potential targets identified in the present study are more reliable than those identified by previous studies.