Glaucocalyxin B Relieving Dyskinesia Inflammation and Oxidative Stress in Parkinson's Disease Model Rats by Activating the NRF2/HO-1 Pathway

To analyze that glaucocalyxin B can alleviate dyskinesia, inflammatory response and oxidative stress in Parkinson's disease model rats by activating the nuclear factor erythroid 2–related factor 2/heme oxygenase-1 pathway. 150 adults were divided into 5 groups, namely, the sham operation group (healthy mice), the Parkinson's group and the low-dose group (Parkinson+20 ng/ml) glaucocalyxin B), the medium-dose group (Parkinson+40 ng/ml glaucocalyxin B) and high-dose group (Parkinson+60 ng/ml glaucocalyxin B). The number of adjustment steps, the number of forepaw movements and the number of positive reactions in each group at 0 d have no difference; on the 3rd d in the Parkinson's group, dose group were reduced than in the sham operation group; on the 7th d, the number of steps in the Parkinson's group, and dose groups were reduced than the sham operation group. The tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6 in the Parkinson's disease group, and dose groups were raised than those in the sham operation group, while these in the dose groups were reduced than in the Parkinson's group. The reactive oxidative stress concentration and myeloperoxidase activity of the Parkinson's group, dose group were raised than those of the sham operation group, while in the dose group were reduced than the Parkinson's group; superoxide dismutase activity level was reduced than the sham operation group. The levels of nuclear factor erythroid 2-related factor and heme oxygenase-1 in the Parkinson's group, dose groups were raised than those in the sham operation group, while in the dose groups were raised than those in the Parkinson's group. Further, in the low, medium and high dose groups increased with the increase of dose (p<0.05). Glaucocalyxin B can alleviate the dyskinesia of Parkinson's disease model rats and reduce the inflammatory response and oxidative stress response in rats, its relevant mechanism via activating the nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway.