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PAIN MECHANISMS

Electroacupuncture Attenuates Bone Cancer Pain and Inhibits Spinal Interleukin-1ß Expression in a Rat Model

Rui-Xin Zhang, PhD^*, Aihui Li, PhD^*, Bing Liu, MD^*, Linbo Wang, BS^*, Ke Ren, PhD, Jian-Tian Qiao, MD, Brian M. Berman, MD^*, and Lixing Lao, PhD^*

From the *Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, Maryland; Department of Biomedical Sciences, Dental School, University of Maryland, Baltimore, Maryland; and Department of Neurobiology, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.

Address correspondence and reprint requests to Dr. Rui-Xin Zhang, Center for Integrative Medicine, University of Maryland, School of Medicine, HSF-2, Room S209, 20 Penn Street, Baltimore, MD 21201. Address e-mail to Rzhan001{at}umaryland.edu.

Abstract

BACKGROUND: Although pain affects the quality of life of cancer patients, current medical treatments are either ineffective or have side effects. In the present study we investigated the effect of electroacupuncture (EA) on cancer-induced hyperalgesia and expression of interleukin-1ß (IL-1ß), upregulation of which is related to the maintenance of persistent pain, in a rat model of bone cancer pain.

METHODS: Cancer was induced by injecting AT-3.1 prostate cancer cells into the tibia of male Copenhagen rats. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min daily at the equivalent of the human acupoint GB30 (Huantiao) between Days 14 and 18 after cancer cell inoculation. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency to a noxious thermal stimulus, was measured at baseline and 20 min after EA treatment. IL-1ß and its mRNA were respectively determined by immunohistochemistry and reverse transcription-polymerase chain reaction analysis.

RESULTS: Thermal hyperalgesia developed between Days 12 and 18 after cancer cell inoculation. EA significantly (P < 0.05) attenuated this hyperalgesia, increasing paw withdrawal latency from 7.0 ± 0.3 s to 9.2 ± 0.4 s, and inhibited the upregulation of IL-1ß and its mRNA compared to the sham control. Intrathecal injection of IL-1 receptor antagonist (IL-1ra, 0.1 mg/rat) also significantly inhibited cancer-induced thermal hyperalgesia.

CONCLUSION: The data suggest that EA alleviates bone cancer pain, at least in part by suppressing IL-1ß expression. The results support the clinical use of EA in the treatment of cancer pain.

Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999