Apigetrin alleviates intervertebral disk degeneration by regulating nucleus pulposus cell autophagy

IF 3.4 3区 医学 Q1 ORTHOPEDICS
JOR Spine Pub Date : 2024-04-17 DOI:10.1002/jsp2.1325
Tao Xu, Hongqi Zhao, Jian Li, Xuan Fang, Hua Wu, Weihua Hu
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Abstract

Background

Intervertebral disk degeneration (IVDD) is a common spine disease, and inflammation is considered to be one of its main pathogenesis. Apigetrin (API) is a natural bioactive flavonoid isolated from various herbal medicines and shows attractive anti-inflammatory and antioxidative properties; whereas, there is no exploration of the therapeutic potential of API on IVDD. Here, we aim to explore the potential role of API on IVDD in vivo and in vitro.

Methods

In vitro, western blotting, real-time quantitative polymerase chain reaction, and immunofluorescence analysis were implemented to explore the bioactivity of API on interleukin-1 beta (IL-1β)-induced inflammatory changes in nucleus pulposus cells (NPCs). In vivo, histological staining and immunohistochemistry were employed to investigate the histological changes of intervertebral disk sections on puncture-induced IVDD rat models.

Results

In vitro, API played a crucial role in anti-inflammation and autophagy enhancement in IL-1β-induced NPCs. API improved inflammation by inhibiting the nuclear factor-kappaB and mitogen-activated protein kinas pathways, whereas it promoted autophagy via the phosphatidylinositol 3-kinase/AKT/mammalian target of the rapamycin pathway. Furthermore, in vivo experiment illustrated that API mitigates the IVDD progression in puncture-induced IVDD model.

Conclusions

API inhibited degenerative phenotypes and promoted autophagy in vivo and in vitro IVDD models. Those suggested that API might be a potential drug or target for IVDD.

Abstract Image

阿匹格林能通过调节髓核细胞自噬缓解椎间盘退变
背景 椎间盘退行性变(IVDD)是一种常见的脊柱疾病,炎症被认为是其主要发病机制之一。芹菜素(API)是从多种中草药中分离出来的一种天然生物活性黄酮类化合物,具有很强的抗炎和抗氧化作用,但目前还没有研究表明芹菜素具有治疗椎间盘突出症的潜力。在此,我们旨在探讨 API 在体内和体外对 IVDD 的潜在作用。 方法 在体外,采用 Western 印迹、实时定量聚合酶链反应和免疫荧光分析方法,探讨原料药对白细胞介素-1β(IL-1β)诱导的髓核细胞(NPCs)炎性变化的生物活性。在体内,采用组织学染色和免疫组化方法研究穿刺诱导的 IVDD 大鼠模型椎间盘切片的组织学变化。 结果 在体外,API 在 IL-1β 诱导的 NPCs 中发挥了抗炎和增强自噬的关键作用。API 通过抑制核因子-kappaB 和丝裂原活化蛋白激酶途径改善炎症,而通过磷脂酰肌醇 3- 激酶/AKT/雷帕霉素哺乳动物靶标途径促进自噬。此外,体内实验表明,在穿刺诱导的 IVDD 模型中,API 可减轻 IVDD 的进展。 结论 在体内和体外 IVDD 模型中,API 可抑制退行性表型并促进自噬。这表明 API 可能是治疗 IVDD 的潜在药物或靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
JOR Spine
JOR Spine ORTHOPEDICS-
CiteScore
6.40
自引率
18.90%
发文量
42
审稿时长
10 weeks
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