| The purpose of this study mainly aims to observe the effects of catalpol in Parkinson's disease model of mice induced by rotenone and its action mechanism.In mice, rotenone could model Parkinson's disease with severe damage to dopaminergic system. Behavioral test performed in Y-maze showed that rotenone depressed the cognition of mice, decreased the contents of dopamine and its metabolization in midbrain and striatum which had been assayed with HPLC. Catalpol (10 mg/kg for 10 days) improved the cognition of mice, increased the content of dopamine and DOPAC in mice midbrain and striatum.In order to make clear the neuroprotective mechanism of catalpol, mitochondrial function and antioxidant/oxidant parameters of mice midbrain and striatum were investigated. The results proved that catalpol improved Complex I and GSH-PX and SOD and ATPase acivities, inhibited LDH activity, reduced the content of ROS, resume mitochondrial membrane potential and GSH content in rotenone-treated mice. All these suggested that catalpol was a potential neuroprotective agent and its neuroprotective effects were achieved at least partly by promoting endogenous antioxidant enzymatic activities and inhibiting free radical generation and modulating brain mitochondrial function.Furthermore, the splenic weights and the activities of endogenous antioxidants and the content of lipid peroxide in spleen and liver were assayed. The results proved that catalpol significantly elevated the splenic weights, increased the levels of GSH, GSH-PX and SOD, decreased GST activity and MDA level of mice. All these suggested that catalpol could protect spleen and liver from rotenone-induced damage by modulating immunity status and promoting endogenous antioxidant enzymatic activities.It could be concluded that catalpol protected rotenone induced PD mice from damage and may exert its protection by modulating brain mitochondrial function, promotmg endogenous antioxidant enzymatic activities and improving immunity status.
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