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电针可减轻大鼠模型中的骨癌疼痛并抑制脊髓白细胞介素-1β表达。

Electroacupuncture attenuates bone cancer pain and inhibits spinal interleukin-1 beta expression in a rat model.

作者信息

Zhang Rui-Xin, Li Aihui, Liu Bing, Wang Linbo, Ren Ke, Qiao Jian-Tian, Berman Brian M, Lao Lixing

机构信息

Center for Integrative Medicine, School of Medicine, University of Maryland, Baltimore, Maryland 21201, USA.

出版信息

Anesth Analg. 2007 Nov;105(5):1482-8, table of contents. doi: 10.1213/01.ane.0000284705.34629.c5.

DOI:10.1213/01.ane.0000284705.34629.c5
PMID:17959986
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-1beta (IL-1beta), 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-1beta 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-1beta 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-1beta expression. The results support the clinical use of EA in the treatment of cancer pain.

摘要

背景

尽管疼痛会影响癌症患者的生活质量,但目前的医学治疗要么无效,要么有副作用。在本研究中,我们在骨癌疼痛大鼠模型中研究了电针(EA)对癌症诱导的痛觉过敏以及白细胞介素-1β(IL-1β)表达的影响,IL-1β的上调与持续性疼痛的维持有关。

方法

通过将AT-3.1前列腺癌细胞注射到雄性哥本哈根大鼠的胫骨中诱导癌症。在接种癌细胞后的第14天至18天,每天在相当于人体穴位GB30(环跳)处用10 Hz/2 mA/0.4 ms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,即对有害热刺激的爪退缩潜伏期缩短。通过免疫组织化学和逆转录-聚合酶链反应分析分别测定IL-1β及其mRNA。

结果

在接种癌细胞后的第12天至18天出现热痛觉过敏。电针显著(P < 0.05)减轻了这种痛觉过敏,使爪退缩潜伏期从7.0 +/- 0.3秒增加到9.2 +/- 0.4秒,并且与假对照相比,抑制了IL-1β及其mRNA的上调。鞘内注射IL-1受体拮抗剂(IL-1ra,0.1 mg/大鼠)也显著抑制了癌症诱导的热痛觉过敏。

结论

数据表明,电针至少部分通过抑制IL-1β表达来减轻骨癌疼痛。这些结果支持电针在癌症疼痛治疗中的临床应用。

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