Gastrodin alleviates Tourette syndrome via Nrf-2/HO-1/HMGB1/NF-kB pathway

The aim is to study the effects of gastrodin (GA) on striatal inflammation and oxidative stress in rats with Tourette syndrome (TS). The rat model of TS was induced by 3,3 '-iminodipropionitrile. Behavioral tests were carried out by stereotype experiment. The concentrations of amino acid transmitters glutamic acid (Glu) and gamma-aminobutyric acid (GABA) in striatum were determined by high-performance liquid chromatography. Superoxide dismutase (SOD) and malondialdehyde (MDA) in serum and striatum were detected by commercial kits. Cytokines in serum and striatum were detected by enzyme-linked immunosorbent assay kits. Western blot analysis was used to detect striatum nuclear erythroid factor 2-related factor 2 (Nrf-2)/heme oxygenase-1 (HO-1)/high mobility group box 1 protein (HMGB1)/nuclear factor-kB (NF-kB) pathway-related proteins. The expressions of Nrf-2 and P-NF-kBp65 in striatum were detected by immunohistochemistry. Compared with the control group, the stereotype scores of rats in the model group significantly increased, and the contents of Glu and GABA in striatum obviously increased. GA significantly reduced the stereotype scores and decreased the contents of Glu and GABA. The levels of SOD in serum and striatum were decreased and the content of MDA in serum and striatum were increased compared with the control group, while GA significantly restored the changes. GA significantly adjusted Nrf-2/HO-1/HMGB1/NF-kB pathway-related proteins changes consistent with immunohistochemical changes. GA may protect striatum of rats with TS by regulating Nrf-2/HO-1/HMGB1/NF-kB pathway protein changes in striatum.