Depression is one of main symptoms accompanying thermal hyperalgesia and mechanical allodynia induced by inflammatory pain. On physiological level, depressive symptoms could be attenuated by sufficient level of hippocampal neural plasticity. Adult hippocampal neurogenesis (AHN) plays critical roles in clearing panic memory, increasing psychiatric adaptability and preventing depressive emotion. Thus, targeting AHN is the applicable strategy to improve neural functions impaired and attenuate inflammatory pain. Previous reports indicate natural compound baicalin (BA) is one of the effective agents to promote AHN. In present study, we tested the effects of BA in mouse model of inflammatory pain as well as its biological underpinning. Behavioral tests indicate that BA treatment attenuated thermal hyperalgesia, mechanical allodynia and depressive symptoms. Meanwhile, treatment of BA promoted growth and differentiation of neural stem cells in hippocampus. AHN blocker temozolomide (TMZ) resulted in significant suppressed effects of BA to promote AHN, suggesting the critical role of AHN in regulating behavioral effects of BA to inflammatory pain. Akt plays the critical roles in the effects of BA to attenuate inflammatory pain induced symptoms. Prohibiting of Akt with GSK960693 dramatically prevented the effects of BA in attenuating inflammatory pain induced behavioral symptoms. Taken together, BA is the potential pain killer to alleviating inflammatory pain via Akt-mediated adult hippocampal neurogenesis.
Keywords: Adult hippocampal neurogenesis; Akt pathway; Baicalin; Depressive symptom; Inflammatory pain.