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姜黄素通过调控Bcl-2/Bax保护大鼠终板软骨细胞免受白细胞介素-1β诱导的细胞凋亡。

Curcumin protects rat endplate chondrocytes against IL-1β-induced apoptosis via Bcl-2/Bax regulation.

作者信息

Wan Chao, Liu Shixing, Zhao Long, Chang Chengbing, Li Hewen, Li Rui, Chen Bin

机构信息

Department of Orthopedics, Chengde Central Hospital, Chengde, 067000, Heibei, China.

The 981 Hospital of the Joint Service Support Force of the Chinese People's Liberation Army, Chengde, 067000, Heibei, China.

出版信息

J Mol Histol. 2025 Mar 19;56(2):111. doi: 10.1007/s10735-025-10390-x.

Abstract

The study aims to investigate the protective effect of curcumin on intervertebral disc degeneration by examining its influence on IL-1β-induced apoptosis in rat cartilage endplate cells. The rat primary chondrocytes treated by IL-1 β at 10 ng /mL was utilized as a rat model in intervertebral disc degeneration, followed by incubation with different concentration of curcumin (10, 15, 20 μmol/L). Cell apoptosis and cell proliferation were conducted through flow cytometry and CCK-8, respectively. Furthermore, immunofluorescence staining was used to visualize the expression of Bax and Bcl-2 inside the cells. Western blotting was performed to determine the expression of the Bax and Bcl-2. Curcumin promoted proliferation of chondrocytes treated by IL-1 β, but inhibited the apoptosis. Importantly, curcumin significantly downregulated the expression level of Bax but upregulated the expression level of Bcl-2. Strengths of this study include the use of multiple assays to validate the findings, while limitations include the in vitro nature and lack of in vivo data. Curcumin is capable of ameliorating IL-1β -induced intervertebral disc degeneration by Bcl-1 and Bax production. This study provides a foundation for future research into curcumin's therapeutic potential in intervertebral disc degeneration.

摘要

该研究旨在通过检测姜黄素对白细胞介素-1β(IL-1β)诱导的大鼠软骨终板细胞凋亡的影响,来探讨姜黄素对椎间盘退变的保护作用。将用10 ng/mL的IL-1β处理的大鼠原代软骨细胞用作椎间盘退变的大鼠模型,然后用不同浓度(10、15、20 μmol/L)的姜黄素进行孵育。分别通过流式细胞术和CCK-8检测细胞凋亡和细胞增殖情况。此外,采用免疫荧光染色观察细胞内Bax和Bcl-2的表达情况。通过蛋白质免疫印迹法检测Bax和Bcl-2的表达。姜黄素促进了经IL-1β处理的软骨细胞的增殖,但抑制了细胞凋亡。重要的是,姜黄素显著下调了Bax的表达水平,但上调了Bcl-2的表达水平。本研究的优点包括使用多种检测方法来验证研究结果,而局限性包括实验性质为体外实验且缺乏体内数据。姜黄素能够通过调节Bcl-1和Bax的产生来改善IL-1β诱导的椎间盘退变。本研究为未来研究姜黄素在椎间盘退变中的治疗潜力奠定了基础。

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