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技术文章
系统性红斑狼疮的发病触发髓核细胞热下垂，加剧椎间盘退变
点击次数：2686 发布时间：2025/1/23 22:18:59
2024年10月，浙江中医药大学附属医院（浙江省中医医院）骨科创伤研究所；杭州富阳中医骨科创伤医院；浙江中医药大学附属医院（浙江省中医医院）骨科；浙江中医药大学基础医学院(Institute of Orthopaedics and Traumatology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang, 310053, People’s Republic of China; Hangzhou Fuyang Hospital of TCM Orthopedics and Traumatology, Hangzhou, Zhejiang, 311400, People’s Republic of China; Department of Orthopaedics, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang, 310053, People’s Republic of China;College of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, 310053, People’s Republic of China)Hongting Jin老师研究团队在《Journal of Inflammation Research》上发表论文：
“The Onset of Systemic Lupus Erythematosus Triggers Nucleus Pulposus Cell Pyroptosis to Exacerbate Intervertebral Disc Degeneration”
“系统性红斑狼疮的发病触发髓核细胞热下垂，加剧椎间盘退变”
Abstract：
Purpose
Systemic lupus erythematosus (SLE) is an autoimmune disorder marked by immune system dysregulation and autoantibodies production, causing widespread inflammation and damage across various body systems. Despite the prevalent back pain in SLE patients, the link between SLE and intervertebral disc (IVD) degeneration, a primary contributor to back pain, remains inadequately understood. This study explored the impact of SLE on IVD degeneration using the MRL/lpr mouse model, which effectively replicates human SLE manifestations.
Methods
The study utilized MRL/lpr mice to investigate the effects of SLE on IVD degeneration. The mice were evaluated for typical SLE phenotypes and indicators of IVD degeneration, including IVD height, IVD score, tissue integrity, extracellular matrix degradation, and apoptosis of IVD cells. Additionally, the study examined nucleus pulposus (NP) pyroptosis and inflammatory cytokine secretion. Mechanistic analysis focused on the antioxidant pathway, specifically the expression levels of NRF2, HO-1, KEAP1, and the phosphorylation levels of p65.
Results
MRL/lpr mice displayed typical SLE phenotypes and exacerbated profiles of IVD degeneration, including reduced IVD height, lower IVD score, significant IVD tissue impairment, extracellular matrix degradation, and increased apoptosis of IVD cells. Notably, SLE stimulated NP pyroptosis and excessive secretion of inflammatory cytokines. Mechanistic analysis indicated that the progression of SLE impedes the antioxidant pathway by downregulating NRF2 and HO-1 expression, upregulating KEAP1, and enhancing phosphorylation levels of p65.
Conclusion
Our findings highlight the mechanistic link between SLE and IVD degeneration, suggesting potential therapeutic targets for mitigating back pain in SLE patients.
摘要：
目的：
系统性红斑狼疮（SLE）是一种以免疫系统失调和自身抗体产生为特征的自身免疫性疾病，可引起全身各系统的广泛炎症和损伤。尽管SLE患者普遍存在背痛，但SLE与椎间盘退变（IVD）之间的联系仍未充分了解，椎间盘退变是背痛的主要原因。本研究通过MRL/lpr小鼠模型探索SLE对IVD变性的影响，该模型有效地复制了人类SLE的表现。
方法：
本研究利用MRL/lpr小鼠研究SLE对IVD变性的影响。评估小鼠的典型SLE表型和IVD变性指标，包括IVD高度、IVD评分、组织完整性、细胞外基质降解和IVD细胞凋亡。此外，研究还检测了髓核（NP）焦亡和炎症细胞因子分泌。机制分析侧重于抗氧化途径，特别是NRF2、HO-1、KEAP1的表达水平和p65的磷酸化水平。
结果：
MRL/lpr小鼠表现出典型的SLE表型，IVD退化加剧，包括IVD高度降低、IVD评分降低、IVD组织损伤明显、细胞外基质降解和IVD细胞凋亡增加。值得注意的是，SLE刺激NP焦亡和炎性细胞因子的过量分泌。机制分析表明，SLE的进展通过下调NRF2和HO-1的表达，上调KEAP1，提高p65的磷酸化水平，从而阻碍了抗氧化途径。
结论：
我们的研究结果强调了SLE和IVD变性之间的机制联系，提出了缓解SLE患者背痛的潜在治疗靶点。
该论文中，Rat NP cell line (rNPCs)的体外培养是使用Ausbian特级胎牛血清完成的。
原创作者：北京缔一生物科技有限公司
