The impact of the opioids fentanyl and morphine on nociception and bone destruction in a murine model of bone cancer pain

2007 ◽  
Vol 87 (1) ◽  
pp. 30-40 ◽  
Author(s):  
Mohammed El Mouedden ◽  
Theo Frans Meert
Keyword(s):  
Cancer Pain ◽  
Murine Model ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
The Impact

Bone cancer pain model in mice: evaluation of pain behavior, bone destruction and morphine sensitivity

2004 ◽  
Vol 79 (2) ◽  
pp. 243-251 ◽  
Author(s):  
Hilde Vermeirsch ◽  
Rony M. Nuydens ◽  
Philip L. Salmon ◽  
Theo F. Meert
Keyword(s):  
Cancer Pain ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Pain Behavior ◽  
Bone Cancer Pain ◽  
Pain Model

scholarly journals Neurochemical and Cellular Reorganization of the Spinal Cord in a Murine Model of Bone Cancer Pain

1999 ◽  
Vol 19 (24) ◽  
pp. 10886-10897 ◽  
Author(s):  
Matthew J. Schwei ◽  
Prisca Honore ◽  
Scott D. Rogers ◽  
Janeen L. Salak-Johnson ◽  
Matthew P. Finke ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cancer Pain ◽  
Murine Model ◽  
Bone Cancer ◽  
Bone Cancer Pain

scholarly journals Topical Treatment with Xiaozheng Zhitong Paste (XZP) Alleviates Bone Destruction and Bone Cancer Pain in a Rat Model of Prostate Cancer-Induced Bone Pain by Modulating the RANKL/RANK/OPG Signaling

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Yanju Bao ◽  
Yebo Gao ◽  
Maobo Du ◽  
Wei Hou ◽  
Liping Yang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Pain ◽  
Structural Damage ◽  
Bone Pain ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Osteoblast Activity ◽  
Mechanical Threshold ◽  
Bone Damage

To explore the effects and mechanisms of Xiaozheng Zhitong Paste (XZP) on bone cancer pain, Wistar rats were inoculated with vehicle or prostate cancer PC-3 into the tibia bone and treated topically with inert paste, XZP at 15.75, 31.5, or 63 g/kg twice per day for 21 days. Their bone structural damage, nociceptive behaviors, bone osteoclast and osteoblast activity, and the levels of OPG, RANL, RNAK, PTHrP, IGF-1, M-CSF, IL-8, and TNF-αwere examined. In comparison with that in the placebo group, significantly reduced numbers of invaded cancer cells, decreased levels of bone damage and mechanical threshold and paw withdrawal latency, lower levels of serum TRACP5b, ICTP, PINP, and BAP, and less levels of bone osteoblast and osteoclast activity were detected in the XZP-treated rats (P<0.05). Moreover, significantly increased levels of bone OPG but significantly decreased levels of RANL, RNAK, PTHrP, IGF-1, M-CSF, IL-8, and TNF-αwere detected in the XZP-treated rats (P<0.05for all). Together, XZP treatment significantly mitigated the cancer-induced bone damage and bone osteoclast and osteoblast activity and alleviated prostate cancer-induced bone pain by modulating the RANKL/RANK/OPG pathway and bone cancer-related inflammation in rats.

scholarly journals Phosphoproteomic Profiling of Rat’s Dorsal Root Ganglia Reveals mTOR as a Potential Target in Bone Cancer Pain and Electro-Acupuncture’s Analgesia

2021 ◽  
Vol 12 ◽  
Author(s):  
Wen Wang ◽  
You Zhou ◽  
Yangqian Cai ◽  
Sisi Wang ◽  
Fangbing Shao ◽  
...  
Keyword(s):  
Cancer Pain ◽  
Dorsal Root ◽  
Protein Microarray ◽  
Mammalian Target Of Rapamycin ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Mtor Signaling ◽  
Bone Cancer Pain ◽  
Underlying Mechanisms ◽  
Mixed Pain

Bone cancer pain (BCP) is a clinical refractory mixed pain involving neuropathic and inflammatory pain, with the underlying mechanisms remaining largely unknown. Electro-acupuncture (EA) can partly alleviate BCP according to previous research. We aim to explore the proteins and major pathways involved in BCP and EA treatment through phosphoproteomic profiling. BCP rat model was built by tibial inoculation of MRMT-1 mammary gland carcinoma cells. Mechanical hyperalgesia determined by paw withdrawal thresholds (PWTs) and bone destruction manifested on the radiographs confirmed the success of modeling, which were attenuated by EA treatment. The differentially expressed phosphorylated proteins (DEPs) co-regulated by BCP modeling and EA treatment in rat dorsal root ganglions (DRGs) were analyzed through PEX100 Protein microarray. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that DEPs were significantly enriched in mammalian target of rapamycin (mTOR) signaling pathway. The phosphorylations of mTOR at Ser2448 and Thr2446 were increased in BCP and downregulated by EA. In addition, the phosphorylation of S6K and Akt, markers of the mTOR complex, were also increased in BCP and downregulated by EA. Inhibition of mTOR signaling alleviated the PWTs of BCP rats, while the mTOR agonist impaired the analgesic effect of EA. Thus, our study provided a landscape of protein phosphorylation changes in DRGs of EA-treated BCP rats and revealed that mTOR signaling can be potentially targeted to alleviate BCP by EA treatment.

scholarly journals STING suppresses cancer pain via immune and neuronal modulation

2021 ◽  
Author(s):  
Kaiyuan Wang ◽  
Christopher R. Donnelly ◽  
Changyu Jiang ◽  
Yihan Liao ◽  
Xueshu Tao ◽  
...  
Keyword(s):  
Pain Relief ◽  
Cancer Pain ◽  
Immune Cell ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Tumor Burden ◽  
Bone Cancer Pain ◽  
Local Tumor ◽  
Nociceptive Neurons ◽  
Local Bone

AbstractAgonists of the innate immune regulator stimulator of interferon genes (STING) have shown great efficacy in promoting antitumor immunity in preclinical models, leading to their exploration in cancer immunotherapy trials. Patients with advanced stage cancers frequently suffer from severe pain as a result of bone metastasis and bone destruction, for which there is no efficacious treatment. Here, using multiple mouse models of metastatic bone cancer, we report that STING agonists confer remarkable protection against cancer pain, bone destruction, and local tumor burden. Repeated systemic administration of STING agonists robustly attenuated bone cancer-induced pain symptoms and improved locomotor function. Interestingly, STING agonists provided acute pain relief through direct neuronal modulation, as ex vivo incubation of STING agonists reduced excitability of pain-sensing nociceptive neurons from tumor-bearing mice. In addition, STING agonists protected local bone destruction and reduced local tumor burden through modulation of osteoclast and immune cell function in the tumor microenvironment, providing long-term cancer pain relief. Finally, these in vivo effects were dependent on host-intrinsic STING and Ifnar1. Overall, STING activation provides unique advantages in controlling metastatic bone cancer pain through distinct and synergistic actions on nociceptors, immune cells, and osteoclasts.

scholarly journals SB366791, a TRPV1 antagonist, potentiates analgesic effects of systemic morphine in a murine model of bone cancer pain †

2009 ◽  
Vol 102 (2) ◽  
pp. 251-258 ◽  
Author(s):  
Y. Niiyama ◽  
T. Kawamata ◽  
J. Yamamoto ◽  
S. Furuse ◽  
A. Namiki
Keyword(s):  
Cancer Pain ◽  
Murine Model ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Analgesic Effects ◽  
Trpv1 Antagonist

scholarly journals STING suppresses bone cancer pain via immune and neuronal modulation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Kaiyuan Wang ◽  
Christopher R. Donnelly ◽  
Changyu Jiang ◽  
Yihan Liao ◽  
Xin Luo ◽  
...  
Keyword(s):  
Pain Relief ◽  
Cancer Pain ◽  
Cell Function ◽  
Immune Cell ◽  
Bone Destruction ◽  
Bone Cancer ◽  
Tumor Burden ◽  
Bone Cancer Pain ◽  
Local Tumor ◽  
Local Bone

AbstractPatients with advanced stage cancers frequently suffer from severe pain as a result of bone metastasis and bone destruction, for which there is no efficacious treatment. Here, using multiple mouse models of bone cancer, we report that agonists of the immune regulator STING (stimulator of interferon genes) confer remarkable protection against cancer pain, bone destruction, and local tumor burden. Repeated systemic administration of STING agonists robustly attenuates bone cancer-induced pain and improves locomotor function. Interestingly, STING agonists produce acute pain relief through direct neuronal modulation. Additionally, STING agonists protect against local bone destruction and reduce local tumor burden through modulation of osteoclast and immune cell function in the tumor microenvironment, providing long-term cancer pain relief. Finally, these in vivo effects are dependent on host-intrinsic STING and IFN-I signaling. Overall, STING activation provides unique advantages in controlling bone cancer pain through distinct and synergistic actions on nociceptors, immune cells, and osteoclasts.

scholarly journals Decitabine attenuates nociceptive behavior in a murine model of bone cancer pain

Pain ◽  
2019 ◽  
Vol 160 (3) ◽  
pp. 619-631 ◽  
Author(s):  
Camilla Kristine Appel ◽  
Nicole Newell Scheff ◽  
Chi Tonglien Viet ◽  
Brian Lee Schmidt ◽  
Anne-Marie Heegaard
Keyword(s):  
Cancer Pain ◽  
Murine Model ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Nociceptive Behavior

Initial thermal heat hypoalgesia and delayed hyperalgesia in a murine model of bone cancer pain

2003 ◽  
Vol 969 (1-2) ◽  
pp. 102-109 ◽  
Author(s):  
Luis Menéndez ◽  
Ana Lastra ◽  
Manuel F Fresno ◽  
Sara Llames ◽  
Álvaro Meana ◽  
...  
Keyword(s):  
Cancer Pain ◽  
Murine Model ◽  
Bone Cancer ◽  
Bone Cancer Pain
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