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白藜芦醇苷通过维持骨代谢平衡和抑制巨噬细胞极化来延缓骨关节炎的进展。

Polydatin retards the progression of osteoarthritis by maintaining bone metabolicbalance and inhibiting macrophage polarization.

作者信息

Sun Qi, Nan Xin-Yu, Wang Hui, Pan Shuo, Ji Gang, Guo Ya-Feng, Zhao Ya-Heng, Li Gao-Cen, Guo Shao-Shi, Lin Lu-Feng, Jin Yu-Jie, Zhang Xue Li, Liu Chang-Cheng, Liu Guo-Bin

机构信息

The First Hospital of Hebei Medical University, Shijiazhuang, Hebei, China.

Hebei Medical University, Shijiazhuang, Hebei, China.

出版信息

Front Bioeng Biotechnol. 2025 Jan 7;12:1514483. doi: 10.3389/fbioe.2024.1514483. eCollection 2024.

DOI:10.3389/fbioe.2024.1514483
PMID:39840130
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11747576/
Abstract

BACKGROUND

Polydatin (PD), also known as tiger cane glycoside, is a natural compound extracted from the Japanese knotweed plant, which is often referred to as white resveratrol. It exhibits anti-inflammatory, antioxidant, and anti-apoptotic effects in the treatment of various diseases. However, the potential molecular mechanisms of PD in osteoarthritis have not been clearly elucidated.

METHODS

Anterior cruciate ligament transection (ACLT) surgery was performed to establish an osteoarthritis animal model. Female mice at the age of 12 weeks were intraperitoneally injected with different concentrations of PD (20 and 40 mg/kg). models were established by isolating mouse articular chondrocytes, which were subsequently treated with lipopolysaccharide or IL-1β for 24 h for subsequent experiments. In addition, different concentrations of PD were administered for 12 h. Morphological changes were observed by toluidine blue staining, joint bone metabolism changes were observed by tartrate-resistant acid phosphatase staining, immunohistochemistry was used to observe the expression levels of inflammatory factors and extracellular matrix. MicroCT analysis was conducted to assess changes in the microstructure of subchondral bone trabeculae, and Western blot was performed to measure the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway and markers of M1 polarization in macrophages.

RESULTS

PD significantly delays the progression of osteoarthritis induced by ACLT, effectively inhibits IL-1β-induced joint inflammation, bone metabolic remodeling and extracellular matrix degradation. In addition, paeoniflorin markedly suppresses the transmission of the NF-κB signaling pathway and reverses M1 polarization in macrophages induced by IL-1β.

CONCLUSION

Taken together, PD might be a potential therapeutic agent for the prevention and treatment of osteoarthritis.

摘要

背景

虎杖苷(PD),也被称为虎杖糖苷,是从虎杖植物中提取的一种天然化合物,常被称为白藜芦醇。它在治疗各种疾病中表现出抗炎、抗氧化和抗凋亡作用。然而,PD在骨关节炎中的潜在分子机制尚未明确阐明。

方法

进行前交叉韧带横断(ACLT)手术以建立骨关节炎动物模型。对12周龄雌性小鼠腹腔注射不同浓度的PD(20和40mg/kg)。通过分离小鼠关节软骨细胞建立细胞模型,随后用脂多糖或IL-1β处理24小时以进行后续实验。此外,给予不同浓度的PD 12小时。通过甲苯胺蓝染色观察形态学变化,通过抗酒石酸酸性磷酸酶染色观察关节骨代谢变化,采用免疫组织化学观察炎症因子和细胞外基质的表达水平。进行MicroCT分析以评估软骨下骨小梁微观结构的变化,并进行蛋白质印迹法测量活化B细胞核因子κB(NF-κB)信号通路的表达以及巨噬细胞中M1极化的标志物。

结果

PD显著延缓ACLT诱导的骨关节炎进展,有效抑制IL-1β诱导的关节炎症、骨代谢重塑和细胞外基质降解。此外,芍药苷明显抑制NF-κB信号通路的传导,并逆转IL-1β诱导的巨噬细胞M1极化。

结论

综上所述,PD可能是预防和治疗骨关节炎的潜在治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/85cb69472000/fbioe-12-1514483-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/541dc3acfd78/fbioe-12-1514483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/66ae9917b6f4/fbioe-12-1514483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/ad8ca9f5c032/fbioe-12-1514483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/8ff111f3bf06/fbioe-12-1514483-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/23548f64eed9/fbioe-12-1514483-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/800b01b74d87/fbioe-12-1514483-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/93df40fe55ac/fbioe-12-1514483-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/85cb69472000/fbioe-12-1514483-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/541dc3acfd78/fbioe-12-1514483-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/66ae9917b6f4/fbioe-12-1514483-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/ad8ca9f5c032/fbioe-12-1514483-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/8ff111f3bf06/fbioe-12-1514483-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/23548f64eed9/fbioe-12-1514483-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/800b01b74d87/fbioe-12-1514483-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/93df40fe55ac/fbioe-12-1514483-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1f/11747576/85cb69472000/fbioe-12-1514483-g008.jpg

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