DAB can induce oxidative stress and activate microglia, causing neuropathies such as motor and memory deficits (Gagnaire et al., 1991, Kim et al., 2001b).
Growing evidence reports that 1,2-Diacetylbenezene (DAB) is known as a neurotoxic metabolite of 1,2-Diethylbenzene, a white liquid that is a small part of petroleum and engine oil, which causes neuropathy such as hippocampal impairment and proximal axonopathy (Duc Nguyen et al., 2022a, Gagnaire et al., 1991, Kim et al., 2001b, Nguyen et al., 2022b). Thus, upregulation of xenobiotic detoxification genes and related hormones may contribute to cell lifespan by protecting cells against xenobiotic toxicity (Duc Nguyen et al., 2021d, Nguyen et al., 2022, Hoang et al., 2021, Hoffmann and Partridge, 2015). It has been well-known that xenobiotics, nutrition, and pharmaceutical treatments, especially genetics and hormones, have all been shown to influence the aging process (Duc Nguyen et al., 2021a, Duc Nguyen et al., 2021b, Duc Nguyen et al., 2021d, Fontana and Partridge, 2015, Nguyen et al., 2022, Le Couteur et al., 2011, Nguyen et al., 2021b, Nguyen et al., 2022d, Steinbaugh et al., 2012). These findings partly paved the way for further study on the effects of xenobiotics on human health, especially in the aging population. Interestingly, increasing evidence indicates that there are significant differences between young and old rodents related to detoxification and metabolism of xenobiotics (Amador-Noguez et al., 2007, Hoang et al., 2021, Steinbaugh et al., 2012). It has been known that inter-and intraindividual genetic differences among people can modulate the level of harm, primarily by altering xenobiotic metabolism and detoxification outcomes (Abdelsalam et al., 2020). The negative effects of xenobiotics on human health are becoming more widely understood (Duc et al., 2021a, Duc et al., 2021b, Duc Nguyen et al., 2022b, Nguyen et al., 2021a, Nguyen et al., 2022c). These findings will contribute to our understanding of the processes through which prolactin's beneficial effects counteract DAB-induced memory and motor deficits. The most significant transcription factors associated with differentially expressed gene regulation were Six3, Rxrg, Nkx26, and Tbx20. We also identified several key miRNAs associated with memory and motor deficits, as well as prolactin and DAB exposure (rno-miR-141–3p, rno-miR-200a-3p, rno-miR-124–3p, rno-miR-26, and rno-let-7 families). The most important mechanisms associated with prolactin's ability to counteract DAB were identified, including "learning and memory," and "positive regulation of ion transport" in young rats, as well as "acetylcholine related pathways," "inflammatory response pathway," and "neurotransmitter release cycle" in old rats. Co-expression interactions were identified as the most important interactions (83.2 % for young rats and 100 % for old rats). Almost all of these genes were downregulated in both young and old rats given DAB, but they were increased in both young and old rats given prolactin. We observed that prolactin may improve memory and motor deficits caused by DAB via 13 genes (Scn5a, Lmntd1, LOC100360619, Rgs9, Srpk3, Syndig1l, Gpr88, Egr2, Ctxn3, Drd2, Ttr, Gpr6, and Ecel1) in young rats and 9 genes (Scn5a, Chat, RGD1560608, Ucma, Lrrc31, Gpr88, Col1a2, Cnbd1, and Ttr) in old rats. GSE119435), transcriptomic data, GeneMANIA, ToppGeneSuite, Metascape, STRING database, Cytoscape, and Autodock were used as the core tools in in-silico analyses. The gene expression omnibus database (no. We aimed to identify the molecular mechanisms through which prolactin protects against 1,2-Diacetylbenzene (DAB)-induced memory and motor impairments.
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