Senkyunolide H inhibits activation of microglia and attenuates lipopolysaccharide-mediated neuroinflammation and oxidative stress in BV2 microglia cells via regulating ERK and NF-κB pathway.

Neuropathic pain is one of the common surgical diseases, which leads to abnormal chronic pain and pain hypersensitivity reaction. Microglia are important glial cells in the spinal cord, which are conducive to sensitization and maintenance of chronic pain. Recently, Senkyunolide H (SNH) has been reported to play an anti-inflammatory and antioxidant role. However, the mechanisms by which SNH improves neuropathic pain symptoms remain unknown. This study aimed to evaluate and identify the role of SNH in lipopolysaccharide (LPS)-mediated neuroinflammation and oxidative stress in BV2. Western blot and immunostaining assays revealed that SNH treatment attenuated LPS-mediated activation of BV2 in a dose-dependent manner. Flow cytometry further verified that BV2 microglial cells gradually shifted from an M1 (pro-inflammatory) phenotype to an M2 (anti-inflammatory) phenotype after SNH administration. Furthermore, quantitative real-time polymerase chain reaction and ELISA assays demonstrated that SNH treatment attenuated LPS-mediated neuroinflammation and oxidative stress in BV2 microglial cells. Lastly, western blot assays suggested that SHN could inactivate the ERK and NF-κB signaling pathways. Altogether, our findings have demonstrated that SNH could reverse LPS-mediated activation of microglia, LPS-mediated neuroinflammation and oxidative stress in BV2 via regulating the ERK and NF-κB pathways.