Oxymatrine reduces neuropathic pain in diabetic mice through the p38 MAPK/NF-κB signaling pathway.

Diabetic neuropathic pain (DNP) is the most painful complications of diabetes. Oxymatrine (OMT) is one of the main components of Bitter Ginseng (radix Sophorae flavescentis) and has therapeutic effects on many secondary complications associated with diabetes mellitus; however, whether it improves DNP is unknown. The DNP mice model was induced by injecting streptozotocin (STZ) and alterations in body weight, blood glucose, mechanical nociceptive and thermal nociceptive sensitivity were measured over an 8-week period to determine the induction time needed to create DNP mice. OMT were injected intraperitoneally to see how different doses of OMT affected DNP, oxidative and inflammatory responses in diabetic mice. 0.2μg/kg p38 MAPK/NF-κB pathway agonist (P79350) was administered to investigate the influence on the action of OMT and explore the potential mechanism by which OMT alleviates DNP in diabetic mice. The best induction time for generating DNP mice was 4 weeks after continuous injection of 50mg/kg STZ. In mice, OMT effectively attenuated DNP, inhibited oxidative stress and inflammation. OMT inhibited the phosphorylation of pathway proteins p38 and NF-κB p65. However, activating p38 MAPK/NF-κB signaling with P79350 greatly reduced the effect of OMT. OMT attenuates DNP in diabetic mice via inhibiting p38 MAPK/NF-κB signaling.