Gastrodin relieved complete Freund's adjuvant-induced spontaneous pain by inhibiting inflammatory response

- Gastrodin (GAS) relieved chronic inflammatory pain and anxiety-like behaviors induced by Complete Freund's adjuvant (CFA).
- GAS inhibited the enhanced expression of GluR1, GluN2A, GluN2B and CaMKII-α in anterior cingulate cortex (ACC) of CFA-mice.
- GAS administration inhibited the activation of astrocytes and microglia in the ACC of CFA-injected mice.
- GAS treatment reduced the induction of TNF-α and IL-6 in the ACC of CFA-injected mice.

The analgesic effects of gastrodin (GAS), an active component derived from the Chinese herb Tian ma (Gastrodia elata Blume), on chronic inflammatory pain of mice and the involved molecular mechanisms were investigated. GAS significantly attenuated mice chronic inflammatory pain induced by hindpaw injection of complete Freund's adjuvant (CFA) and the accompanying anxiety-like behaviors. GAS administration reduced CFA-induced up-regulation of GluR1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, GluN2A- and GluN2B-containing N-methyl-d-aspartate (NMDA) receptors, and Ca2 +/calmodulin-dependent protein kinase II-alpha (CaMKII-α) in the anterior cingulate cortex (ACC). The GluN2A and GluN2B subunits of NMDA receptors, the GluR1 type of AMPA receptor, and CaMKII-α are key molecules responsible for neuroplasticity involved in chronic pain and the accompanying anxiety. Moreover, GAS administration reduced the activation of astrocyte and microglia and the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice. Therefore, GAS administration relieved chronic pain, exerted anxiolytic effects by regulating neuroplasticity molecules, and attenuated the inflammatory response by reducing the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice.