AI Article Synopsis
- Electroacupuncture (EA) has shown potential in preventing morphine tolerance in rats with bone cancer pain, but the specific mechanism behind this effect is not well understood.
- In the study, researchers observed that EA appears to decrease protein expression of certain signaling molecules (like p-PI3K and p-Akt) in the spinal dorsal horn, which are linked to morphine tolerance development.
- Additionally, the use of a PI3K inhibitor (LY294002) further reduced morphine tolerance, while an insulin-like growth factor (IGF-1) agonist reversed EA's protective effects, indicating a complex interplay in the signaling pathways involved.
Article Abstract
Purpose: Morphine is often used for the treatment of moderate and severe cancer pain, but long-term use can lead to morphine tolerance. Methods for effectively inhibiting morphine tolerance and the related mechanism of action are of great significance for the treatment of cancer pain. Previous studies have shown that electroacupuncture (EA) can inhibit the occurrence of morphine tolerance, but the mechanism is not yet clear. The aim of the present study was to explore the signaling pathway by which EA attenuates the development of bone cancer pain (BCP)-morphine tolerance (MT).
Materials And Methods: Changes in the paw withdrawal threshold (PWT) of rats with bone cancer pain-morphine tolerance were observed in a study of EA combined with intrathecal injection of a PI3K inhibitor (LY294002) or agonist (insulin-like growth factor-1 [IGF-1]). We also tested the protein expression of phosphorylated phosphatidylinositol 3-kinase (p-PI3K), phosphorylated protein kinase B (p-Akt), phosphorylated c-Jun NH-terminal kinase 1/2 (p-JNK1/2), and β-arrestin2 in the L4-6 spinal dorsal horn of rats.
Results: The protein expression of p-PI3K, p-Akt, p-JNK1/2, and β-arrestin2 was upregulated in the L4-6 spinal dorsal horn of rats with bone cancer pain and bone cancer pain-morphine tolerance. EA delayed the occurrence of morphine tolerance in rats with bone cancer pain and downregulated the protein expression of p-PI3K, p-Akt, p-JNK1/2, and β-arrestin2 in the L4-6 spinal dorsal horn of rats with bone cancer pain-morphine tolerance. Intrathecal injection of LY294002 attenuated the development of morphine tolerance and downregulated the protein expression of p-Akt, p-JNK1/2, and β-arrestin2 in the spinal dorsal horn of rats with bone cancer pain-morphine tolerance. In addition, the inhibitory effect of EA on morphine tolerance was reversed by IGF-1.
Conclusion: The mechanism underlying the ability of EA to attenuate morphine tolerance may be associated with inhibition of the PI3K/Akt/JNK1/2 signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8164555 | PMC |
| http://dx.doi.org/10.1177/1534735421995237 | DOI Listing |
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