Swertiamarin alleviates diabetic peripheral neuropathy in rats by suppressing NOXS/ ROS/NLRP3 signal pathway

To observe the therapeutic effect of swertiamarin on diabetic peripheral neuropathy (DPN) in rats and explore the molecular mechanism in light of the NOXS/ROS/NLRP3 signal pathway. Thirty-two SD rats were randomly divided into control group, DPN model group (treated with saline), swertiamarin (5 mg/kg) treatment group and NOXS inhibitor (10 mL/kg DPI) treatment group. Rat models of DPN were established in the latter 3 groups by intraperitoneal injections of STZ, and the treatments were administered on days 1, 7 and 14 after modeling. Tactile hypersensitivity of the rats was evaluated 30 min after the treatment. The expressions of NOXS, ROS, NLRP3 and inflammatory factors in the spinal cord tissue were detected using ELISA, and the protein expressions of NOXS, ROS, and NLRP3 were also detected with Western blotting. Compared with those in the control group, the rats in DPN group showed significant hyperalgesia ( < 0.001), increased expressions of TNF-α ( < 0.001) and IL-6 ( < 0.001), decreased expressions of TGF-β ( < 0.001), and increased expressions of NOXS/ROS/NLRP3 signal pathway ( < 0.001). Compared with those in DPN model group, the rats with swertiamarin treatment showed improved hyperalgesia ( < 0.001), decreased expressions of TNF-α ( =0.03) and IL-6 ( =0.002), increased expressions of TGF-β ( =0.04), and decreased expressions of NOXS ( < 0.001), ROS ( < 0.001) and NLRP3 ( =0.002). Treatment with swertiamarin and the NOXS inhibitor produced similar effects on the expressions of the inflammatory factors in the rat models ( >0.05). DPN effectively relieves hyperalgesia in rat models of DPN by restoring the balance in the expressions of the inflammatory factors by suppressing NOXs/ROS/NLRP3 signaling pathway.