摘要
The rostral ventromedial medulla (RVM) plays a critical role in pain signal transmissions. However, the mechanisms of RVM in type 2 diabetic neuropathy are still poorly understood. Therefore, we evaluated the mechanisms within the RVM in the modulation of neuropathic pain in type 2 diabetes. To this end, we used Zucker diabetic fatty (ZDF) rats to examine the levels of TNF alpha, IL-1 beta, and NF-kappa B in the RVM during the development of neuropathic pain in type 2 diabetes, and evaluated the effects of intra-RVM microinjections of thalidomide on the levels of TNF alpha, IL-1 beta, and NF-kappa B in the RVM and mechanical allodynia and thermal hyperalgesia induced by type 2 diabetes. We found that ZDF rats became hyperglycemic and exhibited increased levels of TNF alpha, IL-1 beta, and NF-kappa B in the RVM at the age of 13 weeks. Intra-RVM administrations of thalidomide dose-dependently attenuated mechanical allodynia and thermal hyperalgesia, and this phenomenon was associated with reduced levels of TNF alpha, IL-1 beta, and NF-kappa B in the RVM, without altering serum levels of TNF alpha or IL-1 beta These results suggested that supraspinal mechanisms of thalidomide play a critical role in modulations of type 2 diabetes induced neuropathic pain, which is likely mediated by TNF alpha and IL-1 beta in the RVM.
- 出版日期2016-7
- 单位中国人民解放军白求恩国际和平医院; 石家庄市第一医院