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

Author:

Zhou Qinfei1,Gong Liyan1ORCID,Bao Guanai2,Ding Qunfang1,Ji Jingjing1

Affiliation:

1. Department of Rare and Head and Neck Oncology, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang 310022, China

2. Rehabilitation Department, The Cancer Hospital of the University of Chinese Academy of Sciences (Zhejiang Cancer Hospital), Institute of Basic Medicine and Cancer (IBMC), Chinese Academy of Sciences, Hangzhou, Zhejiang 310022, China

Abstract

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 μg/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.

Funder

Zhejiang Provincial Medical and Health Scientific and Technical Fund

Publisher

Hindawi Limited

Subject

Applied Mathematics,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,Modeling and Simulation,General Medicine

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