OBJECTIVE: To observe the protective effects of echinacoside on rotenone-induced damages in rats. METHODS: Healthy male Sprague-Dawley rats, weighing from 200 to 220 g, were randomly divided into five groups with 20 rats in each group: control group, rotenone group and echinacoside groups of low, medium and high doses (20, 40 and 80 mg/(kg·d)). Rats in the rotenone group were injected intraperitoneally for four weeks with rotenone (2.75 mg/(kg·d)), dissolved into dimethyl sulfoxide; rats in the control group were injected intraperitoneally with dimethyl sulfoxide daily, and rats in the echinacoside groups received daily intraperitoneal injection of rotenone along with echinacoside gastric perfusion for four weeks. Modified neurological severity score was used to evaluate neurobehavior of the animals; dopaminergic neurons in substantia nigra were observed by immunochemical method and dopamine concentration in striatum was determined by a fluorescence spectrophotometer. Biomarkers of liver and kidney damage were also measured. RESULTS: In the rotenone group, the rats suffered from severe neurological disability (P<0.01), and the number of dopaminergic neurons in substantia nigra and dopamine concentration in striatum were decreased (P<0.05) compared with the normal control group; levels of the biomarkers for evaluating liver and kidney damage were increased (P<0.05). In the echinacoside groups, the neurological disability and the loss of dopaminergic neurons in substantia nigra were suppressed and dopamine concentrations in striatum were increased (P<0.05), but the liver and kidney damage was not improved (P>0.05). CONCLUSION: Rotenone causes severe damages to dopaminergic neurons, liver and kidney in rats and echinacoside selectively reverses dopaminergic neuronal injury.
OBJECTIVE: To observe the protective effects of echinacoside on rotenone-induced damages in rats. METHODS: Healthy male Sprague-Dawley rats, weighing from 200 to 220 g, were randomly divided into five groups with 20 rats in each group: control group, rotenone group and echinacoside groups of low, medium and high doses (20, 40 and 80 mg/(kg·d)). Rats in the rotenone group were injected intraperitoneally for four weeks with rotenone (2.75 mg/(kg·d)), dissolved into dimethyl sulfoxide; rats in the control group were injected intraperitoneally with dimethyl sulfoxide daily, and rats in the echinacoside groups received daily intraperitoneal injection of rotenone along with echinacoside gastric perfusion for four weeks. Modified neurological severity score was used to evaluate neurobehavior of the animals; dopaminergic neurons in substantia nigra were observed by immunochemical method and dopamine concentration in striatum was determined by a fluorescence spectrophotometer. Biomarkers of liver and kidney damage were also measured. RESULTS: In the rotenone group, the rats suffered from severe neurological disability (P<0.01), and the number of dopaminergic neurons in substantia nigra and dopamine concentration in striatum were decreased (P<0.05) compared with the normal control group; levels of the biomarkers for evaluating liver and kidney damage were increased (P<0.05). In the echinacoside groups, the neurological disability and the loss of dopaminergic neurons in substantia nigra were suppressed and dopamine concentrations in striatum were increased (P<0.05), but the liver and kidney damage was not improved (P>0.05). CONCLUSION:Rotenone causes severe damages to dopaminergic neurons, liver and kidney in rats and echinacoside selectively reverses dopaminergic neuronal injury.