PDF(Pubmed)
Abstract：
UNASSIGNED: Traumatic optic neuropathy is known to be a critical condition that can cause blindness; however, the specific mechanism underlying optic nerve injury is unclear. Recent studies have reported that artemisinin, considered vital in malaria treatment, can also be used to treat neurodegenerative diseases; however, its precise role and mechanism of action remain unknown. Therefore, in this study, we aimed to investigate the impact and probable mechanism of action of artemisinin in retinal ganglion cells (RGCs) in a mouse model of traumatic optic neuropathy induced by optic nerve crush (ONC).
UNASSIGNED: ONC was induced in the left eye of mice by short-term clamping of the optic nerve; oral artemisinin was administered daily. The neuroprotective effect of the drug was assessed using Tuj-1 staining in RGCs. In addition, the inflammatory response and the expression levels of phosphorylated tau protein and tau oligomers were observed using RT-qPCR, TUNEL assay, and fluorescence staining to investigate the underlying mechanisms.
UNASSIGNED: Artemisinin increased the survival rate of RGCs 14 days after ONC. Artemisinin significantly reduced the levels of inflammatory factors such as CXCL10, CXCR3, and IL-1β in the retina and decreased the apoptosis of RGCs. Moreover, downregulation of the phosphorylation of tau proteins and the expression of tau oligomers were observed after artemisinin treatment.
UNASSIGNED: Our results suggest that artemisinin can increase the survival rate of RGCs after ONC and reduce their apoptosis. This effect may be achieved by inhibiting the inflammatory response it triggers and downregulating tau protein phosphorylation and tau oligomer expression. These findings suggest the potential application of artemisinin as a therapeutic agent for neuropathy.
UNASSIGNED: ONC was induced in the left eye of mice by short-term clamping of the optic nerve; oral artemisinin was administered daily. The neuroprotective effect of the drug was assessed using Tuj-1 staining in RGCs. In addition, the inflammatory response and the expression levels of phosphorylated tau protein and tau oligomers were observed using RT-qPCR, TUNEL assay, and fluorescence staining to investigate the underlying mechanisms.
UNASSIGNED: Artemisinin increased the survival rate of RGCs 14 days after ONC. Artemisinin significantly reduced the levels of inflammatory factors such as CXCL10, CXCR3, and IL-1β in the retina and decreased the apoptosis of RGCs. Moreover, downregulation of the phosphorylation of tau proteins and the expression of tau oligomers were observed after artemisinin treatment.
UNASSIGNED: Our results suggest that artemisinin can increase the survival rate of RGCs after ONC and reduce their apoptosis. This effect may be achieved by inhibiting the inflammatory response it triggers and downregulating tau protein phosphorylation and tau oligomer expression. These findings suggest the potential application of artemisinin as a therapeutic agent for neuropathy.
摘要：
■已知外伤性视神经病变是一种可导致失明的危重症；然而，视神经损伤的具体机制尚不清楚。最近的研究报道，青蒿素，被认为对疟疾治疗至关重要，也可用于治疗神经退行性疾病;然而，其确切作用和作用机制尚不清楚。因此,在这项研究中，我们旨在研究青蒿素对视神经挤压(ONC)所致外伤性视神经病变小鼠模型视网膜神经节细胞(RGCs)的影响及其可能的作用机制.
■通过短期夹住视神经在小鼠的左眼中诱导ONC；每天口服青蒿素。在RGC中使用Tuj-1染色评估药物的神经保护作用。此外,用RT-qPCR观察炎症反应和磷酸化tau蛋白和tau寡聚体的表达水平,TUNEL检测,和荧光染色，以探讨潜在的机制。
■青蒿素在ONC后14天增加了RGC的存活率。青蒿素能显著降低视网膜中CXCL10、CXCR3、IL-1β等炎症因子的水平，降低RGCs的凋亡。此外，青蒿素处理后，观察到tau蛋白磷酸化和tau寡聚体表达的下调。
■我们的结果表明，青蒿素可以提高ONC后RGC的存活率并减少其凋亡。这种效果可以通过抑制其引发的炎症反应并下调tau蛋白磷酸化和tau寡聚体表达来实现。这些发现表明青蒿素作为神经病的治疗剂的潜在应用。
■通过短期夹住视神经在小鼠的左眼中诱导ONC；每天口服青蒿素。在RGC中使用Tuj-1染色评估药物的神经保护作用。此外,用RT-qPCR观察炎症反应和磷酸化tau蛋白和tau寡聚体的表达水平,TUNEL检测,和荧光染色，以探讨潜在的机制。
■青蒿素在ONC后14天增加了RGC的存活率。青蒿素能显著降低视网膜中CXCL10、CXCR3、IL-1β等炎症因子的水平，降低RGCs的凋亡。此外，青蒿素处理后，观察到tau蛋白磷酸化和tau寡聚体表达的下调。
■我们的结果表明，青蒿素可以提高ONC后RGC的存活率并减少其凋亡。这种效果可以通过抑制其引发的炎症反应并下调tau蛋白磷酸化和tau寡聚体表达来实现。这些发现表明青蒿素作为神经病的治疗剂的潜在应用。
