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It is shown that great progress was recently made in the treatment of repetitive transcranial magnetic stimulation (rTMS) for neurological and psychiatric diseases. This study aimed to address how rTMS exerted it therapeutic effects by regulating competitive endogenous RNAs (ceRNAs) of lncRNA-miRNA-mRNA. The distinction of lncRNA, miRNA and mRNA expression in male status epilepticus (SE) mice treated by two different ways, low-frequency rTMS (LF-rTMS) vs. sham rTMS, was analyzed by high-throughput sequencing. The Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out. Gene–Gene Cross Linkage Network was established; pivotal genes were screened out. qRT-PCR was used to verify gene–gene interactions. Our results showed that there were 1615 lncRNAs, 510 mRNAs, and 17 miRNAs differentially which were expressed between the LF-rTMS group and the sham rTMS group. The expression difference of these lncRNAs, mRNAs, and miRNAs by microarray detection were consistent with the results by qPCR. GO functional enrichment showed that immune-associated molecular mechanisms, biological processes, and GABA-A receptor activity played a role in SE mice treated with LF-rTMS. KEGG pathway enrichment analysis revealed that differentially expressed genes were correlated to T cell receptor signaling pathway, primary immune deficiency and Th17 cell differentiation signaling pathway. Gene–gene cross linkage network was established on the basis of Pearson’s correlation coefficient and miRNA. In conclusion, LF-rTMS alleviates SE through regulating the GABA-A receptor activity transmission, improving immune functions, and biological processes, suggesting the underlying ceRNA molecular mechanisms of LF-rTMS treatment for epilepsy.

It is shown that much advances were made in the treatment of repetitive transcranial magnetic stimulation (rTMS) for neurological and psychiatric diseases in recent years studies. This study aimed to reveal how rTMS exerts it therapeutic effects by regulating competitive endogenous RNAs (ceRNAs) of lncRNA-miRNA-mRNA. The distinction in lncRNA, miRNA and mRNA expression between low-frequency rTMS-treated male SE mice and male SE mice treated with sham rTMS were analyzed by high-throughput sequencing. The Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out. Gene-Gene Cross Linkage Network was established, and pivotal genes were screened out. qRT-PCR was used to verify gene-gene interactions. In short, there were 1615 lncRNAs, 510 mRNAs and 17 miRNAs differentially expressed between the low-frequency rTMS group and the sham rTMS group. The expression difference of these lncRNAs, mRNAs, and miRNAs by microarray detection were consistent with the resutls by qPCR. GO functional enrichment showed that immune-associated molecular mechanisms and biological processes, GABA-A receptor activity play a role in SE mice treated with low-frequency rTMS. As revealed by KEGG pathway enrichment analysis, differentially expressed genes are correlated to T cell receptor signaling pathway, primary immune deficiency and Th17 cell differentiation signaling pathway. Gene -gene cross linkage network was established on the basis of Pearson's correlation coefficient and miRNA. In conclusion, LF-rTMS alleviates SE through regulating the GABA-A receptor activity transmission, improving immune functions and biological processes, implicating that LF-rTMS may be a viable therapeutic option for epilepsy.

Purpose: This study was to explore whether Ginkgo biloba extract (GBE) improve memory impairment by alleviating neuroinflammation signaling in mice with status epilepticus. Methods:The status epilepticus (SE) mice model was established by pilocarpine and treated with 100 mg / kg of GBE for 14 days. Spontaneous alternation of Y-maze and new object recognition were used to explore memory impairment. To examine glial cell activation, we performed immunohistochemistry and immunofluorescence staining. The activation of NF-κB signaling and the expression level of lncRNA-COX2 were detected by Western blot and qRT-PCR, respectively. Adeno-associated virus lncRNA-COX2 was injected into mice for overexpression of lncRNA-COX2.Results: After GBE treatment, the spontaneous alternation rate and the recognition coefficient in SE mice were both increased. Moreover, activation of glial cells, NF-κB signaling and lncRNA-COX2 were significantly decreased in SE mice.In the GBE-treated SE mice with lncRNA-COX2 overexpression, NF-κB signaling was up-regulated again; the reduced level of inflammation factors was reversed; the GBErescued spontaneous alternation rate of Y-maze was eliminated. Conclusion:Our results suggested that GBE reduces the hippocampal inflammation by down-regulating lncRNA-COX2 / NF-κB signaling in the SE mice, leading to the decrease of neuronal damage and the improvement of memory functions.

Introduction Schizophrenia's heritability and familial transmission have been known for several decades. The male‐specific Y chromosome plays an important role in schizophrenia. Short tandem repeats (STRs)have been recognized as risk genes in the development of schizophrenia. Here, we investigated the association between male schizophrenia and Y‐chromosomal STRs loci. Methods We recruited 355 patients with schizophrenia and 473 healthy males for physical examination and amplified them with a PowerPlex 21 System fluorescence‐labeled composite amplification System. Then, the resultant products were separated by electrophoresis and further detected. Finally, differences in allele and genotype frequency distributions of STR loci were observed. Results Our results showed that all 20 STR loci were in accordance with Hardy–Weinberg's law ( p > .05). There were statistically significant differences in alleles of D13S317 and D5S818 loci and genotype frequency distribution between the two groups (alleles: p = .039, p = .022, respectively; genotype: p = .0004, p = .011, respectively). However, there was no difference in the other autosomal 18 STR loci between the two groups ( p > .05). Univariate analysis showed that the frequency distribution differences of allele 11 and genotype 10‐11 at the D13S317 locus between the two groups were significant (compared to the controls, p = 0.005, odds ratio (OR) = 1.37, 95%b confidence interval (CI) = 1.10–1.71, compared to the controls, p = .0000002, OR = 3.92, 95% CI = 2.27–6.77, respectively). The frequency distribution differences of allele 7 and genotype 7‐10 at D5S818 between the two groups were significant (compared to the controls, p = .0006, OR = 3.42, 95% CI = 1.63–7.16, compared to the controls, p = .0011, OR = 8.24, 95% CI = 1.83–37.05, respectively). Conclusion Polymorphisms of the D13S317 and D5S818 loci may be predisposing factors for schizophrenia.