Knocking down Trim47 ameliorated sevoflurane-induced neuronal cell injury and cognitive impairment in rats

Zhu, Yingjun; Zhang, Min; Wang, Jiayu; Wang, Qingxiu

doi:10.1007/s00221-023-06602-z

Cited by 1 publication

(1 citation statement)

References 24 publications

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“…Silencing Trim47 could inhibit the NF-κB signaling pathway, mitigate inflammatory responses, suppress neuronal cell apoptosis, and ameliorate sevoflurane-induced neuronal cell injury and cognitive dysfunction in neonatal rats. 30 Meanwhile, TRIM47 expression in the brain and vasculature was inversely correlated with the severity of a wide range of small vessel diseases. 31 Furthermore, reducing Trim47 expression in vitro and in vivo has protective effects against cerebral IRI.…”

Section: Discussionmentioning

confidence: 99%

RNA Sequencing Analyses Reveal the Potential Anti-Inflammatory Mechanisms of Acacetin Against ODG/R Injuries in Microglia

Bu,

Mahan,

Zhang

et al. 2024

JIR

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Background Acacetin is a natural flavonoid known for its anti-tumor, antioxidant, and anti-inflammatory properties. Our previous studies have shown its protective effects against cerebral ischemia-reperfusion injury (IRI), but the underlying molecular mechanisms remain unclear. Purpose The study delves into acacetin’s mechanism in mitigating cerebral IRI, with a focus on transcriptomic insights. Methods We established the oxygen-glucose deprivation/re-oxygenation (OGD/R) model in BV2 microglia, treating them with 10μM acacetin. Then we assessed cell proliferation using CCK-8 and measured Lactate Dehydrogenase (LDH) release. High-throughput RNA sequencing (RNA-seq) underpinned the analysis of differentially expressed genes (DEGs) and long non-coding RNAs (lncRNAs), functional enrichment, and alternative splicing events (ASEs), validated by reverse transcription–quantitative polymerase chain reaction (RT-qPCR). Results OGD/R injury significantly impaired cell proliferation and increased LDH release, effects mitigated by acacetin. RNA-seq identified 2148 upregulated and 2135 downregulated DEGs post-OGD/R. In contrast, the acacetin-treated group showed 248 upregulated and 240 downregulated DEGs compared to the OGD/R group. All DEGs were enriched in both Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Overlapping analysis indicated that acacetin treatment reversed the expression of 203 genes affected by OGD/R, including inflammation-related genes such as Isg15, Fcgr1, Il1b, and Parp12. Moreover, the oxidative stress-related gene, Mt2, was downregulated post-OGD/R but upregulated following acacetin treatment. We further found that OGD/R and acacetin treatment could modulate gene splicing events, impacting cell apoptosis or inflammatory responses, such as the A3SS splicing event in the Trim47 gene. RNA-seq also highlighted differential expression of numerous lncRNAs, particularly the upregulation of lncRNA Rmrp and Terc post-OGD/R and their subsequent downregulation post-acacetin treatment. These lncRNAs might regulate cell proliferation through mediating target gene expressions. RT-qPCR validation confirmed these findings. Conclusion Significant upregulation of genes and ASEs linked to oxidative stress and inflammatory response is observed in cerebral IRI. Acacetin intervention reverses these effects, highlighting its mechanism in alleviating the injury by modulating gene expression and splicing events.

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Section: Discussionmentioning

confidence: 99%