Zhang Rui-Xin, Li Aihui, Liu Bing, Wang Linbo, Xin Jiajia, Ren Ke, Qiao Jian-Tian, Berman Brian M, Lao Lixing
Center For Integrative Medicine, School of Medicine, University of Maryland, HSF-2, Room S209, 20 Penn Street, Baltimore, MD 21201, USA.
Eur J Pain. 2008 Oct;12(7):870-8. doi: 10.1016/j.ejpain.2007.12.006. Epub 2008 Jan 24.
Cancer pain impairs the quality of life of cancer patients, but opioid intervention can cause significant side effects that further decrease quality of life. Although electroacupuncture (EA) has been used to treat cancer pain, its mechanisms are largely unknown. To examine its effects and underlying mechanisms on cancer pain, we injected AT-3.1 prostate cancer cells into the tibia to induce bone cancer in the male Copenhagen rat. The resulting pain was treated with 10Hz/2mA/0.4ms pulse EA for 30min daily at the point equivalent to the human acupoint GB30 (Huantiao) between days 14 and 18 after the injection. For sham control, EA needles were inserted into GB30 without stimulation. Thermal hyperalgesia, a decrease in paw withdrawal latency (PWL) to a noxious thermal stimulus, and mechanical hyperalgesia, a decrease in paw withdrawal pressure threshold (PWPT), was measured at baseline and 20min after the EA treatment. Preprodynorphin mRNA and dynorphin were determined by RT-PCR and immunohistochemistry, respectively. Thermal and mechanical hyperalgesia developed ipsilaterally between days 12 and 18 after cancer cell inoculation. EA significantly (P<0.05) attenuated this hyperalgesia, as shown by increased PWL and PWPT, and inhibited up-regulation of preprodynorphin mRNA and dynorphin compared to sham control. Intrathecal injection of antiserum against dynorphin A (1-17) also significantly inhibited the cancer-induced hyperalgesia. These results suggest that EA alleviates bone cancer pain at least in part by suppressing dynorphin expression, and they support the clinical use of EA in the treatment of cancer pain.
癌痛会损害癌症患者的生活质量，但阿片类药物干预会引发严重的副作用，进而进一步降低生活质量。尽管电针（EA）已被用于治疗癌痛，但其机制在很大程度上尚不清楚。为了研究其对癌痛的影响及潜在机制，我们将AT-3.1前列腺癌细胞注射到雄性哥本哈根大鼠的胫骨中以诱发骨癌。在注射后第14天至18天，每天在相当于人体穴位GB30（环跳）的部位给予10Hz/2mA/0.4ms脉冲电针治疗30分钟，以治疗由此产生的疼痛。作为假对照，将电针插入GB30但不进行刺激。在基线和电针治疗后20分钟测量热痛觉过敏（对有害热刺激的爪退缩潜伏期（PWL）缩短）和机械性痛觉过敏（爪退缩压力阈值（PWPT）降低）。分别通过逆转录聚合酶链反应（RT-PCR）和免疫组织化学法测定前强啡肽原mRNA和强啡肽。在癌细胞接种后第12天至18天，同侧出现热痛觉过敏和机械性痛觉过敏。与假对照相比，电针显著（P<0.05）减轻了这种痛觉过敏，表现为PWL和PWPT增加，并抑制了前强啡肽原mRNA和强啡肽的上调。鞘内注射抗强啡肽A（1-17）抗血清也显著抑制了癌症诱导的痛觉过敏。这些结果表明，电针至少部分地通过抑制强啡肽表达来减轻骨癌疼痛，并且支持电针在癌痛治疗中的临床应用。
