Wang Li-na, Yang Jian-ping, Ji Fu-hai, Wang Xiu-yun, Zuo Jian-ling, Xu Qi-nian, Jia Xiao-ming, Zhou Jing, Ren Chun-guang, Li Wei
Department of Anesthesiology, the First Hospital Affiliated to Suzhou University, Suzhou 215006, China.
Zhonghua Yi Xue Za Zhi. 2011 May 10;91(17):1188-92.
To investigate the role of brain-derived neurotrophic factor (BDNF) in pain facilitation and spinal mechanisms in the rat model of bone cancer pain.
The bone cancer pain model was developed by inoculated Walker 256 mammary gland carcinoma cells into the tibia medullary cavity. Sixty SD female rats were divided into 5 groups (n = 12 each) randomly; group I: control group (sham operation); group II: model group; group III: control group + anti-BDNF intrathecal (i.t.); group IV: model group + control IgG i.t.; group V: model group + anti-BDNF i.t.. Anti-BDNF or control IgG was injected i.t. during 7 to 9th day. Von-Frey threshold was measured one day before operation and every 2 days after operation. On the 9th day after threshold tested, rats were sacrificed after i.t. injection of either anti-BDNF or control IgG, the lumbar 4-6 spinal cord was removed. The expression of the spinal BDNF and the phosphorylation of extracellular signal-regulated protein kinase 1/2 (p-ERK1/2) were detected by immunohistochemistry assay and Western-Blot. Co-expression pattern of BDNF and p-ERK1/2 were determined by double-labeling immunofluorescence.
We demonstrated the coexistence of BDNF and p-ERK1/2 in the spinal cord of rats. From the 7 to 9th day after operation, von-Frey threshold in groups II and IV was significantly lower than that in group I and group V (P < 0.01), group V was remarkly higher than that in group IV (P < 0.01). The spinal BDNF and p-ERK1/2 expression in group II or IV were significantly increased compared with that in group I or V (P < 0.01), intrathecal anti-BDNF was significantly suppressed BDNF and p-ERK1/2 expression (P < 0.01).
BDNF and p-ERK1/2 was coexistence in the spinal cord of rats, and it maybe involved in the bone cancer pain.
探讨脑源性神经营养因子（BDNF）在大鼠骨癌痛模型中痛觉易化及脊髓机制中的作用。
通过将Walker 256乳腺癌细胞接种至胫骨骨髓腔建立骨癌痛模型。60只SD雌性大鼠随机分为5组（每组n = 12）；Ⅰ组：对照组（假手术）；Ⅱ组：模型组；Ⅲ组：对照组 + 鞘内注射抗BDNF；Ⅳ组：模型组 + 鞘内注射对照IgG；Ⅴ组：模型组 + 鞘内注射抗BDNF。在第7至9天鞘内注射抗BDNF或对照IgG。术前1天及术后每2天测量von-Frey阈值。在阈值测试后的第9天，鞘内注射抗BDNF或对照IgG后处死大鼠，取出腰4 - 6脊髓。通过免疫组织化学检测和蛋白质印迹法检测脊髓BDNF的表达及细胞外信号调节蛋白激酶1/2（p-ERK1/2）的磷酸化。通过双标免疫荧光法确定BDNF和p-ERK1/2的共表达模式。
我们证实了BDNF和p-ERK1/2在大鼠脊髓中共存。术后第7至9天，Ⅱ组和Ⅳ组的von-Frey阈值显著低于Ⅰ组和Ⅴ组（P < 0.01），Ⅴ组显著高于Ⅳ组（P < 0.01）。Ⅱ组或Ⅳ组脊髓BDNF和p-ERK1/2的表达与Ⅰ组或Ⅴ组相比显著增加（P < 0.01），鞘内注射抗BDNF可显著抑制BDNF和p-ERK1/2的表达（P < 0.01）。
BDNF和p-ERK1/2在大鼠脊髓中共存，可能参与骨癌痛。
