Transcriptome Sequencing Explores the Mechanism of Baicalin on Bone Cancer Pain

Wang, Aitao; Guo, Dongmei; Cheng, Hongyu; Jiang, Hui; Liu, Xiaojuan; Yun, Zhizhong

doi:10.2147/jir.s336028

Cited by 8 publications

(7 citation statements)

References 28 publications

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“…The commonly used bone cancer pain-MT models are mainly femoral or tibial cancer pain-MT models [ 25 ]. Tumor cells inoculated into bone cancer pain models include osteolytic NCTC2472 fibrosarcoma cells [ 26 ], AT-3.1 prostate cancer cells [ 27 ], MADB106 breast cancer cells, and Lewis lung cancer cells [ 20 , 28 ]. In this study, the injection of MADB106 breast cancer cells and morphine (10 mg/kg) was used to establish a metastatic bone cancer pain model.…”

Section: Discussionmentioning

confidence: 99%

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β-Elemene Improves Morphine Tolerance in Bone Cancer Pain via N-Methyl-D-Aspartate Receptor 2B Subunit-Mediated μ-Opioid Receptor

Zhou

Gong

Bao

et al. 2022

Computational and Mathematical Methods in Medicine

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Background Improving morphine tolerance (MT) is an urgent problem in the clinical treatment of bone cancer pain. Considering that β -Elemene is widely used in the treatment of cancer pain, we explored the effects and mechanism of β -Elemene in preventing MT of bone cancer pain. Method Bone cancer pain and chronic MT rat model was established by injecting MADB106 cells and morphine (10 mg/kg). SH-SY5Y cells were treated with morphine (10 μ g/mL) for 48 h to establish a cell model. The mechanical withdrawal threshold and thermal withdrawal latency of rats were detected by mechanical allodynia and thermal hyperalgesia tests, respectively. The protein expressions of μ -opioid receptor (MOPR), cyclic adenosine monophosphate (cAMP), N-methyl-D-aspartate receptor subunit 2B (NR2B), phosphorylated-calmodulin-dependent protein kinase II (p-CaMKII), and CaMKII were detected by western blot. The viability of SH-SY5Y cells was determined by the cell counting kit-8 assay. cAMP content in SH-SY5Y cells was measured by a LANCE cAMP kit. Result Animal experiments showed that MT strengthened over time, while increased β -Elemene dosage alleviated MT. The viability of SH-SY5Y cells was down-regulated by high-dose β -Elemene. In the rat and cell models, long-term morphine treatment decreased the expression of MOPR and increased the cAMP and NR2B expressions and p-CaMKII/CaMKII, while β -Elemene and siNR2B counteracted the effects of morphine treatment. In addition, siNR2B reversed the effects of β -Elemene on related protein expressions and cAMP content in the cell model. Conclusion β -Elemene improved MT in bone cancer pain through the regulation of NR2B-mediated MOPR.

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Section: Discussionmentioning

confidence: 99%

“…A bone cancer pain model was established using the rats following previously described methodologies [ 19 , 20 ]. Briefly, pentobarbital sodium (P-010, Supelco, USA) at a dose of 60 mg/kg was intraperitoneally injected into rats.…”

Section: Methodsmentioning

confidence: 99%

β-Elemene Improves Morphine Tolerance in Bone Cancer Pain via N-Methyl-D-Aspartate Receptor 2B Subunit-Mediated μ-Opioid Receptor

Zhou

Gong

Bao

et al. 2022

Computational and Mathematical Methods in Medicine

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“…CCI is commonly used in model of sciatic nerve injury to explore the pathogenesis of NP. Previous studies have reported that SPP1 is involved in the progression of multiple types of pain 14–16 . Moreover, SPP1 is associated with nerve injury 30,31 .…”

Section: Discussionmentioning

confidence: 98%

“…Previous studies have reported that SPP1 is involved in the progression of multiple types of pain. [14][15][16] Moreover, SPP1 is associated with nerve injury. 30,31 SPP1 is a key regulatory factor that affects nerve degeneration and regeneration after sciatic nerve injury.…”

Section: Discussionmentioning

confidence: 99%

“…Due to cell adhesion, SPP1 expression is closely related to tumorigenesis and metastasis, suggesting that it can be used as a diagnostic and prognostic biomarker of cancer 11–13 . Moreover, SPP1 is associated with multiple types of pain, such as diabetic NP, cancer pain, and low back pain 14–16 . Importantly, a previous study has revealed that SPP1 expression is increased after sciatic nerve injury and regulating nerve degeneration and regeneration 17 .…”

Section: Introductionmentioning

confidence: 99%

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Silencing of secreted phosphoprotein 1 attenuates sciatic nerve injury‐induced neuropathic pain: Regulating extracellular signal‐regulated kinase and neuroinflammatory signaling pathways

Xie,

Lu,

et al. 2024

Immunity Inflam & Disease

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BackgroundNeuropathic pain (NP) is a chronic pathological pain that affects the quality of life and is a huge medical burden for affected patients. In this study, we aimed to explore the effects of secreted phosphoprotein 1 (SPP1) on NP.MethodsWe established a chronic constriction injury (CCI) rat model, knocked down SPP1 via an intrathecal injection, and/or activated the extracellular signal‐regulated kinase (ERK) pathway with insulin‐like growth factor 1 (IGF‐1) treatment. Pain behaviors, including paw withdrawal threshold (PWT), paw withdrawal latency (PWL), lifting number, and frequency, were assessed. After sacrificing rats, the L4‐L5 dorsal root ganglion was collected. Then, SPP1 levels were determined using quantitative polymerase chain reaction (qPCR) and western blot analysis. The levels of interleukin (IL)‐1β, tumor necrosis factor (TNF)‐α, IL‐6, IL‐10, epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF)‐β were determined using qPCR and enzyme‐linked immunosorbent assay. The levels of ERK pathway factors were determined via western blot analysis.ResultsWe found that CCI decreased PWT and PWL, increased the lifting number and frequency, and upregulated SPP1 levels. The loss of SPP1 reversed these CCI‐induced effects. Additionally, CCI upregulated IL‐1β, TNF‐α, IL‐6, EGF, and VEGF levels, downregulated TGF‐β levels, and activated the ERK pathway, while silencing of SPP1 abrogated these CCI‐induced effects. Moreover, IGF‐1 treatment reversed the effects of SPP1 loss.ConclusionsThe data indicate that silencing SPP1 attenuates NP via inactivation of the ERK pathway, suggesting that SPP1 may be a promising target for NP treatment.

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Peripheral Mechanism of Cancer-Induced Bone Pain

Yang,

Zhang

et al. 2023

Neurosci. Bull.

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Transcriptome Sequencing Explores the Mechanism of Baicalin on Bone Cancer Pain

Cited by 8 publications

References 28 publications

β-Elemene Improves Morphine Tolerance in Bone Cancer Pain via N-Methyl-D-Aspartate Receptor 2B Subunit-Mediated μ-Opioid Receptor

β-Elemene Improves Morphine Tolerance in Bone Cancer Pain via N-Methyl-D-Aspartate Receptor 2B Subunit-Mediated μ-Opioid Receptor

Silencing of secreted phosphoprotein 1 attenuates sciatic nerve injury‐induced neuropathic pain: Regulating extracellular signal‐regulated kinase and neuroinflammatory signaling pathways

Peripheral Mechanism of Cancer-Induced Bone Pain

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