Effect of oridonin on oxidative stress parameters inexperimental parkinson's mouse model

Parkinson's disease, caused by the progressive loss of dopaminergic neurons, is the second most common neurodegenerative disease in the world. There is no known definitive treatment except symptomatic treatment with L-dopa therapy, but the existence of various treatment methods is always being investigated in order to increase the life quality of patients. Oridonin obtained from Rabdosia rubescens is a compound with various pharmacological and biological activities such as anti-inflammatory, antibacterial and antitumoral. In several studies examining its effect on Alzheimer, it has been reported that oridonin prevents synaptic losses, improves spatial learning and memory disorders. However, its effect against the damage induced with MPTP in PC12 cells was investigated and it was found that oridonin decreased the number of reactive oxygen species, increased the glutathione level, increased antioxidant enzyme activities. In this study, we aimed to investigate the effect of oridonin on motor and non-motor symptoms and oxidative stress in MPTP-induced Parkinson's mouse model. For this, 8-10 weeks old, C57BL/6 male mice (n=6) were divided into 3 groups: 1) Sham group was given only oridonin solvent, 2) MPTP group was given MPTP (intraperitoneal) to form Parkinson's disease model, 3 The MPTP+oridonin group was first given MPTP to create a Parkinson's disease model, then 10 mg/kg oridonin was given for 15 days. Motor symptoms and bradykinesia were evaluated with the rotarod performance test and stick test, and anxiety and depression with the elevated plus maze test and open field test. At the end of the experiment, SOD, GSHPx, Nrf-2 and MDA levels in striatum tissue were determined by ELISA method. Cell numbers and cellular deterioration were examined by hematoxylineosin staining in the striatum and substantia nigra regions In our results, it was determined that oridonin treatment did not have a curative effect on locomotor activity, anxiety and depression-like behaviors in the Parkinson's mouse model, but antioxidant levels increased and oxidative damage markers decreased in the oridonin treatment group compared to the MPTP group. Our histopathological findings showed that neurophagia and degeneration were observed in the neurons of MPTP-treated mice, there was a significant decrease in the number of cells in the substantia nigra and striatum, and neurophagia was not observed in the MPTP+oridonin group, but milder neuronal degeneration was observed in the MPTP group. As a result, it has been shown that oridonin cannot provide a significant improvement in motor and non-motor symptoms of Parkinson's, but it can reduce oxidative stress and be a neuroprotective agent against damage caused by oxidative stress.