Suppr超能文献

使用英夫利昔单抗阻断 TNF-α 可减轻去卵巢大鼠的机械性和热痛觉过敏。

Blocking TNF-α with infliximab alleviates ovariectomy induced mechanical and thermal hyperalgesia in rats.

机构信息

Department of Orthopaedics, The First Affiliated Hospital of Sun Yat-sen University, 58 Zhongshan second Road, Guangzhou, 510080, China.

出版信息

Neurol Sci. 2012 Jun;33(3):527-33. doi: 10.1007/s10072-011-0743-9. Epub 2011 Aug 27.

Abstract

Studies have proved an increased expression of tumor necrosis factor alpha (TNF-α) in estrogen deficiency animals, and TNF-α also plays a role in inflammation and neuropathic pain. This study aimed to explore the relationship between TNF-α and ovariectomy induced hyperalgesia. 36 female Sparague-Dawley were included, estrogen depletion models were established by ovariectomy. Then infliximab (a TNF-α blocker) was administrated to the ovariectomized rats for 8 weeks. Pain behavioral tests were performed once a week. The bone mineral density (BMD), serum estradiol and TNF-α level were determined at the 8th week after ovariectomy. The expression of TNF-α in lumbar 5 dorsal root ganglions (L5 DRGs) was examined by immunofluorescence method. Significant hyperalgesia to mechanical and thermal stimuli in groups Ovx-1 and Ovx-2 was observed 1 week after the operation. After treated with infliximab, the pain threshold of Ovx-2 was partially restored, although still lower than the Sham group. The serum TNF-α level of Ovx-1 was significantly higher than Sham and Ovx-2. TNF-α immunofluorescence indicated a significant increase in the expression of TNF-α at L5 DRGs in group Ovx-1 when compared with groups Sham and Ovx-2. The BMD of group Ovx-2 was significantly higher than group Ovx-1 and lower than group Sham. In conclusion, TNF-α plays an important role in estrogen deficiency induced mechanical and thermal hyperalgesia, and DRG may be one site on which TNF-α acts to cause hyperalgesia. Blocking the effect of TNF-α could partially alleviate the estrogen deficiency induced hyperalgesia in rats. Thus, TNF-α may contribute to chronic pain in postmenopausal women.

摘要

研究证明,肿瘤坏死因子-α(TNF-α)在雌激素缺乏动物中表达增加,TNF-α在炎症和神经病理性疼痛中也发挥作用。本研究旨在探讨 TNF-α与卵巢切除诱导性痛觉过敏的关系。纳入 36 只雌性 Sprague-Dawley 大鼠,通过卵巢切除术建立雌激素耗竭模型。然后对卵巢切除大鼠给予英夫利昔单抗(TNF-α 阻滞剂)治疗 8 周。每周进行一次疼痛行为测试。卵巢切除后第 8 周测定骨密度(BMD)、血清雌二醇和 TNF-α水平。通过免疫荧光法检测腰椎 5 背根神经节(L5 DRG)中 TNF-α的表达。术后 1 周,Ovx-1 和 Ovx-2 组对机械和热刺激的痛觉明显增强。用英夫利昔单抗治疗后,Ovx-2 组的痛阈部分恢复,尽管仍低于 Sham 组。Ovx-1 组的血清 TNF-α水平明显高于 Sham 和 Ovx-2 组。TNF-α免疫荧光显示,与 Sham 和 Ovx-2 组相比,Ovx-1 组 L5 DRG 中 TNF-α的表达明显增加。Ovx-2 组的 BMD 明显高于 Ovx-1 组,低于 Sham 组。总之,TNF-α在雌激素缺乏诱导的机械性和热痛觉过敏中起重要作用,DRG 可能是 TNF-α引起痛觉过敏的作用部位之一。阻断 TNF-α的作用可部分缓解大鼠雌激素缺乏引起的痛觉过敏。因此,TNF-α可能导致绝经后妇女的慢性疼痛。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验