Bulleyaconitine A prevents Ti particle‐induced osteolysis via suppressing NF‐κB signal pathway during osteoclastogenesis and osteoblastogenesis

Zhang, Liwei; Feng, Min; Li, Zhiyan; Zhu, Min; Fan, Yongyong; Chu, Binxiang; Yuan, Chiting; Chen, Lihua; Lv, Haiyan; Hong, Zhenghua; Hong, Dun

doi:10.1002/jcp.26508

Cited by 11 publications

(7 citation statements)

References 37 publications

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“…In comparison with sandblasted/acid-etched material, sandblasted Ti showed a more significant amount of particle release, possibly due to a significant occurrence of protein-related inflammation and a critical bone loss for in vivo assays. Additionally, Zhang et al [ 25 ] analyzed this using a natural analgesic and anti-inflammation drug (Bulleyaconitine or BLA) to prevent osteolysis induced by Ti particles. When Ti particles in contact with the bone were embedded with BLA, bone resorption decreased by suppressing osteoclast formation and stimulating osteoblast differentiation and mineralization.…”

Section: Introductionmentioning

confidence: 99%

A Tribological and Ion Released Research of Ti-Materials for Medical Devices

et al. 2021

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The increase in longevity worldwide has intensified the use of different types of prostheses for the human body, such as those used in dental work as well as in hip and knee replacements. Currently, Ti-6Al-4V is widely used as a joint implant due to its good mechanical properties and durability. However, studies have revealed that this alloy can release metal ions or particles harmful to human health. The mechanisms are not well understood yet and may involve wear and/or corrosion. Therefore, in this work, commercial pure titanium and a Ti-6Al-4V alloy were investigated before and after being exposed to a simulated biological fluid through tribological tests, surface analysis, and ionic dissolution characterization by ICP-AES. Before exposure, X-ray diffraction and optical microscopy revealed equiaxed α-Ti in both materials and β-Ti in Ti-6Al-4V. Scratch tests exhibited a lower coefficient of friction for Ti-6Al-4V alloy than commercially pure titanium. After exposure, X-ray photoelectron spectroscopy and surface-enhanced Raman spectroscopy results showed an oxide film formed by TiO2, both in commercially pure titanium and in Ti-6Al-4V, and by TiO and Al2O3 associated with the presence of the alloys. Furthermore, inductively coupled plasma atomic emission spectroscopy revealed that aluminum was the main ion released for Ti-6Al-4V, giving negligible values for the other metal ions.

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Section: Introductionmentioning

confidence: 99%

A Tribological and Ion Released Research of Ti-Materials for Medical Devices

et al. 2021

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“…It is reported that BLA suppressed osteoclast formation and bone resorption by inhibiting the NF-κB signal pathway ( Zhang et al, 2018 ). Therefore, we further investigated whether BLA has an impact on fracture healing.…”

Section: Resultsmentioning

confidence: 99%

Bulleyaconitine A reduces fracture-induced pain and promotes fracture healing in mice

et al. 2023

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A fracture is a severe trauma that causes dramatic pain. Appropriate fracture pain management not only improves the patient’s subjective perception, but also increases compliance with rehabilitation training. However, current analgesics for fracture pain are unsatisfactory because of their negative effects on fracture healing or addiction problems. Bulleyaconitine A (BLA), a non-addictive analgesic medicine, is used for the treatment of chronic pain of musculoskeletal disorders in clinical practice, whereas the effects of BLA on fracture pain is undefined. To evaluate the analgesic effects of BLA on fracture, we generated tibial fracture mice here. It is found that oral administration of BLA to mice alleviates fracture-induced mechanical and thermal hyperalgesia. Interestingly, BLA significantly increases locomotor activity levels and reduces anxiety-like behaviors in fractured mice, as determined by open-field test. Notably, BLA treatment promotes bone mineralization and therefore fracture healing in mice, which may be attributed to the increase in mechanical stimulation caused by exercise. Our study suggests that BLA can be used as a promising analgesic agent for the treatment of fracture pain.

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“…In addition, the MAPKs, NF-κB and AKT signaling pathways have been called the most classic signaling pathways in osteoclast formation. In the classic pathway of NF-κB, phosphorylation of IκBα induces the release of the RelA(p65)/p50 heterodimer, which causes nuclear translocation of p65 and ultimately leads to the activation of NF-κB 33 . In this study, we found that EGFL6 enhanced the phosphorylation of IκBα and subsequently the phosphorylation of p65, which means that EGFL6 promoted osteoclast differentiation in part by activating NF-κB and downstream c-Fos/NFATc1 signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

EGFL6 Promotes Bone Metastasis of Lung Adenocarcinoma by Enhancing Osteoclast Differentiation and Stimulating Cancer Cell Metastasis

Song¹,

Xu²,

Jin

et al. 2022

Preprint

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Background Lung cancer is still the most fatal cancer today with approximately 30%-40% of these patients will develop bone metastasis. Lung adenocarcinoma (LUAD) is the most common and aggressive type of lung cancer. The relationship between LUAD and bone metastasis and its underlying mechanism remains unclear. This study proved that epidermal growth factor-like domain multiple 6 (EGFL6) was highly expressed in LUAD specimens of patients, and the expression level was positively correlated with bone metastasis of LUAD. Method The expression of EGFL6 in cancer tissues was detected by IHC. CCK-8, colony formation assay, migration and invasion assay, wound healing assay, immunocytochemistry, RT-PCR, Western blotting, ELISA, bone resorption, TRAP staining and H&E staining were performed. A nude mouse model of LUAD-induced bone destruction was established by injecting A549 cells in different EGFL6 expression levels. Results EGFL6 is elevated in LUAD and is associated with bone metastasis. In vivo, implantation of human adenocarcinoma A549 cells with a higher expression of EGFL6 not only increased tumor growth rate but also bone resorption of tibias in nude mice. In vitro, the secretion of EGFL6 from A549 cells increased osteoclast differentiation but had little effect on osteogenic differentiation. To reveal the underlying mechanism, we demonstrated that EGFL6 enhanced osteoclast differentiation through activating nuclear factor-kappa B (NF-κB) and downstream c-Fos/NFATc1 signaling pathways, and in addition promoted the proliferation, migration and invasion of A549 cells through enhancing the epithelial mesenchymal transformation (EMT) and promoting Wnt/β-catenin and PI3K/AKT/mTOR signaling pathways. Conclusions We unveil EGFL6 as a predictor in bone metastasis of LUAD and underscore the relevance of EGFL6 as a therapeutic target.

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Bulleyaconitine A prevents Ti particle‐induced osteolysis via suppressing NF‐κB signal pathway during osteoclastogenesis and osteoblastogenesis

Cited by 11 publications

References 37 publications

A Tribological and Ion Released Research of Ti-Materials for Medical Devices

A Tribological and Ion Released Research of Ti-Materials for Medical Devices

Bulleyaconitine A reduces fracture-induced pain and promotes fracture healing in mice

EGFL6 Promotes Bone Metastasis of Lung Adenocarcinoma by Enhancing Osteoclast Differentiation and Stimulating Cancer Cell Metastasis

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