长非编码RNA Snhg16 减少臭氧对慢性收缩损伤小鼠的治愈作用通过microRNA-719/SCN1A轴
Jianning Yue1, Qi Wang2, Wenxing Zhao2
1Department of Pain Management, Xuanwu Hospital, Capital Medical University, 45, Changchun Street, Xicheng District, Beijing, 100053, China. yuejn@163.com.
Molecular biotechnology
|August 26, 2023
概括
长非编码RNA Snhg16通过与miR-719相互作用来促进神经病痛 (NP),从而上调SCN1A. 这一轴影响了小鼠对NP的臭氧疗法的有效性.
科学领域:
- 神经科学是一个神经科学.
- 分子生物学分子生物学
- 遗传学 遗传学 是一个
背景情况:
- 神经病痛 (NP) 是一种衰弱的疾病,通常与神经炎症有关.
- 臭氧治疗显示了NP治疗的潜力,但其机制需要阐明.
- 长非编码RNAs (lncRNAs) 在各种生物过程中发挥关键作用,包括疼痛.
研究的目的:
- 研究lncRNA Snhg16在神经病痛 (NP) 中的作用及其与臭氧治疗的相互作用.
- 阐明Snhg16在NP开发中的分子机制.
- 在NP和臭氧处理的背景下探索Snhg16/miR-719/SCN1A轴.
主要方法:
- 慢性收缩损伤 (CCI) 的小鼠模型用于NP诱导.
- 行为测试 (PWT,PLN,PWL) 来评估疼痛反应.
- 针对神经炎症和基因表达的ELISA和qRT-PCR分析.
- 生物信息学,双露西法酶记者测定和RNA拉下用于机制验证.
主要成果:
- 在CCI小鼠中,Snhg16表达升高,加剧了NP并阻碍了臭氧治疗的疗效.
- Snhg16充当了miR-719的分子海绵,SCN1A被确定为miR-719的目标.
- 抑制miR-719可以逆转Snhg16诱导的疼痛行为和神经炎症.
- SCN1A上调部分抵消了miR-719.9的保护作用.
结论:
- 在CCI小鼠中,lncRNA Snhg16通过Snhg16/miR-719/SCN1A通路促进NP的进展.
- 这个分子轴对NP的臭氧治疗的治疗效果产生负面影响.
- 针对Snhg16/miR-719/SCN1A轴为NP处理提供了一个潜在的策略.
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