School of Clinical Medicine, Guizhou Medical University, Guizhou, Guiyang, P. R. China.
Department of Neurosurgery, The Affiliated Hospital of Guizhou Medical University, Guizhou, Guiyang, P. R. China.
Bioengineered. 2021 Dec;12(1):3455-3466. doi: 10.1080/21655979.2021.1947443.
Primary hippocampal neuronal cells were used to establish cell model of cerebral ischemia under oxygen-glucose deprivation (OGD) treatment. After the cell model was pre-treated with short hairpin (sh)-circ_NLRP1 or mmu-miR-199b-3p inhibitor, LDH release and cell apoptosis were detected by LDH kit and TUNEL staining, respectively, while the expression of NLRP3 pyroptosis-related makers was analyzed through immunofluorescence (IF) assay and Western blot, respectively. The binding sites between circ_NLRP1 and mmu-miR-199b-3p were predicted and further validated by Dual Luciferase Reporter assay. Additionally, mitogen-activated protein kinase (MAPK) pathway was also analyzed by means of Western blot assay. Neuronal cells under OGD conditions released less lactate dehydrogenase (LDH) and showed less apoptosis status by silencing circ_NLRP1. In addition, gasdermin D (GSDMD)-N immunofluorescence staining showed weaker fluorescence intensity and decreased expression of pyroptosis-related mediators. We further found that mmu-miR-199b-3p-inhibitor could alter the effects of sh-circ_NLRP1 on hippocampal neuronal cells. In addition, in this process, extracellular signal-regulated kinase (ERK)/EGR1 pathway was also significantly affected. In conclusion, OGD stimulation induced neuronal damage and pyroptosis through enhancing circ_NLRP1 expression and further downregulating mmu-miR-199b-3p levels. The present study provided a novel insight for understanding the potential mechanism of ischemia-induced neuronal damage and for developing new drugs for treating brain ischemia damage.
原代海马神经元细胞用于建立氧葡萄糖剥夺(OGD)处理下的脑缺血细胞模型。在细胞模型用短发夹(sh)-circ_NLRP1 或 mmu-miR-199b-3p 抑制剂预处理后,通过 LDH 试剂盒和 TUNEL 染色分别检测 LDH 释放和细胞凋亡,同时通过免疫荧光(IF)测定和 Western blot 分别分析 NLRP3 细胞焦亡相关标志物的表达。预测 circ_NLRP1 和 mmu-miR-199b-3p 之间的结合位点,并通过双荧光素酶报告基因实验进一步验证。此外,还通过 Western blot 分析了丝裂原活化蛋白激酶(MAPK)通路。沉默 circ_NLRP1 可减少 OGD 条件下神经元细胞释放的乳酸脱氢酶(LDH),减少细胞凋亡状态。此外,GSDMD-N 免疫荧光染色显示荧光强度减弱,细胞焦亡相关介质表达减少。我们进一步发现,mmu-miR-199b-3p 抑制剂可以改变 sh-circ_NLRP1 对海马神经元细胞的影响。此外,在此过程中,细胞外信号调节激酶(ERK)/EGR1 通路也受到显著影响。总之,OGD 刺激通过增强 circ_NLRP1 的表达并进一步下调 mmu-miR-199b-3p 水平,诱导神经元损伤和细胞焦亡。本研究为理解缺血诱导的神经元损伤的潜在机制以及开发治疗脑缺血损伤的新药提供了新的见解。