Résumé
Background: YBX2 and JHDM2A gene is important in spermatogenesis which acts as biomarkers of infertility. Allethrin chemicals widely used in mosquito and potentially toxic drugs that can damage DNA. The purpose of this study was to decide the effect of allethrin on decreasing YBX2 and JHDM2A gene expression on spermatogenesis of male white mice.Methods: This research is an experimental post-test randomized control group design. Twenty-eight rats were given exposure according to the experimental group is K (control), P1 (exposure 4hours), P2 (exposure 8hours), and P3 (exposure 12hours) for 30 days. Examination of YBX2 and JHDM2A gene expression from testicular tissue using real-time PCR with a relatively quantitative calculation method. Research implementation at Animal House and Biomedical Laboratory. Data analysis using one way ANOVA with a significant level of p<0.05.Results: The results of this study were found mean differences amount of YBX2 and JHDM2A gene expression. The mean expression of the control group YBX2 gene is 1.1376, P1: 0.8976, P2: 0.5504, and P3: 0.4512. While in JHDM2A gene control group was 1.7033, P1: 1,7025, P2: 0.6863, and P3: 0.4077. Results of statistical tests using one-way ANOVA is YBX2 (p = 0.010) and JHDM2A (p = 0.000).Conclusions: Based on the results of this study it was concluded that there was an allethrin effect on the decrease in YBX2 and JHDM2A gene expression in the Wistar Albino Rattus novergicus strain.
Résumé
BACKGROUND: Tauopathies, a class of neurodegenerative diseases that includes Alzheimer's disease (AD), are characterized by the deposition of neurofibrillary tangles composed of hyperphosphorylated tau protein in the human brain. As abnormal alterations in histone acetylation and methylation show a cause and effect relationship with AD, we investigated the role of several Jumonji domain-containing histone demethylase (JHDM) genes, which have yet to be studied in AD pathology. METHODS: To examine alterations of several JHDM genes in AD pathology, we performed bioinformatics analyses of JHDM gene expression profiles in brain tissue samples from deceased AD patients. Furthermore, to investigate the possible relationship between alterations in JHDM gene expression profiles and AD pathology in vivo, we examined whether tissue-specific downregulation of JHDM Drosophila homologs (kdm) can affect tauR406W-induced neurotoxicity using transgenic flies containing the UAS-Gal4 binary system. RESULTS: The expression levels of JHDM1A, JHDM2A/2B, and JHDM3A/3B were significantly higher in postmortem brain tissue from patients with AD than from non-demented controls, whereas JHDM1B mRNA levels were downregulated in the brains of patients with AD. Using transgenic flies, we revealed that knockdown of kdm2 (homolog to human JHDM1), kdm3 (homolog to human JHDM2), kdm4a (homolog to human JHDM3A), or kdm4b (homolog to human JHDM3B) genes in the eye ameliorated the tauR406W-engendered defects, resulting in less severe phenotypes. However, kdm4a knockdown in the central nervous system uniquely ameliorated tauR406W-induced locomotion defects by restoring heterochromatin. CONCLUSION: Our results suggest that downregulation of kdm4a expression may be a potential therapeutic target in AD.