长链非编码RNA-Paupar在局麻药致神经毒性过程中的作用研究
The Role of Long Chain Non-coding RNA-Paupar in the Process of Bupivacaine Induced Neurotoxicity
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摘要: 目的 观察长链非编码RNA-Paupar(lnc-Paupar)在布比卡因诱导的神经毒性过程中的调控作用。方法 分离培养小鼠脊髓背根神经节细胞并构建布比卡因神经毒性细胞模型,实时荧光定量PCR(qRT-PCR)观察lnc-Paupar表达,构建lnc-Paupar特异的siRNA-P及随机对照组siRNA-C,200 nmol/L的siRNA-P、siRNA-c转染神经节细胞成功后,通过TUNEL法观察两组细胞凋亡率,Western blot观察JNK及磷酸化JNK(p-JNK)蛋白表达。结果 lnc-Paupar在布比卡因诱导的神经毒性过程表达增高( P<0.05),与siRNA-C组相比,siRNA-P组细胞凋亡率降低( P<0.05)。同时,siRNA-P组抑制细胞JNK及p-JNK蛋白表达( P<0.05)。结论 Lnc-Paupar通过JNK通路产生致神经毒性作用。Abstract: ObjectiveTo observe the expression mode and modulation effects of lncRNA-Paupar in the process of bupivacaine induced neurotoxicity. MethodsDorsal root ganglion (DRG) neurons were cultured and neurotoxicity model was produced on it. And the expression of lncRNA-Paupar was evaluated by qRT-PCR. Lnc-Paupar specific siRNA-P and random control group siRNA-C were constructed, 200 nmol/L siRNA-P, siRNA-C were transfected into ganglion cells and the apoptosis rate of transfected cells were observed by TUNEL method. The JNK and phosphorylated JNK (p-JNK) protein expression were observed with Western blot, respectively. ResultsLncRNA-Paupar was significantly up-regulated during the process of bupivacaine induced neurotoxicity and siRNA mediated lncRNA-Paupar down-regulation protected DRG neurons cells from apoptosis. Both JNK and p-JNK protein were reduced in siRNA transfected cells exemplified by Western blot. ConclusionLncRNA-Paupar could induced neurotoxicity through JNK pathway.
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