Immunopotentiator thymosin alpha-1 attenuates inflammatory pain by modulating the Wnt3a/β-catenin pathway in spinal cord.

Neuroreport2020PMID: 31764244

View on PubMed DOI: 10.1097/WNR.0000000000001370

Plain Language Summary

Thymosin alpha-1 was found to reduce inflammatory pain in a rat model by suppressing the Wnt3a/beta-catenin signaling pathway in the spinal cord. Treatment alleviated both mechanical sensitivity and heat-related pain responses caused by injection of an inflammation-inducing agent. The pain relief was accompanied by reduced levels of key inflammatory molecules including interferon-gamma and tumor necrosis factor-alpha.

Abstract

The mechanism of inflammatory pain involves the central nervous system (CNS) and the immune system. It is reported that immunopotentiator thymosin alpha-1 (Tα1) can reduce inflammation, protect neurons and strengthen the immune function. However, the roles of Tα1 in inflammatory pain still remain unclear. In this study, we found Tα1 can attenuate the complete Freund's adjuvant (CFA)-induced mechanical allodynia and heat hyperalgesia. Meanwhile, it reduced the upregulation of CFA-induced inflammatory mediators (interferon (IFN)-γ, tumor necrosis factor-α and brain-derived neurotrophic factor). In addition, we found the Wnt3a/β-catenin pathway was activated in spinal cord after the injection of CFA, paralleling with pain hypersensitivity. However, Tα1 reversed this status. In summary, Tα1 could attenuate inflammatory pain by modulating the Wnt3a/β-catenin pathway. It might be related to the downregulation of inflammatory mediators.

Authors

Huang, Jiahua; Jiang, Huaqing; Pan, Meijun; Jiang, Yanjun; Xie, Lijin