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Published on: October 26, 2010
Fisetin Improved Rotenone-Induced Behavioral Deficits, Oxidative Changes, and Mitochondrial Dysfunctions in Rat Model
Kanakalatha Alikatte1, Suresh Palle2, Jadi Rajendra Kumar3
1Department of Pharmacology, St. Peters Institute of Pharmaceutical Sciences, Warangal, Telangana, India.
Abstract:
Oxidative stress plays an important role in the pathogenesis of Parkinson's disease (PD), particularly the inhibition of mitochondrial complex-I. This study aimed to evaluate the effect of fisetin in the rotenone-induced rat model of PD. Rotenone was administered (2 mg/kg s.c.) for 35 days to induce PD in animals. Fisetin was administered at two doses (10 mg/kg and 20 mg/kg p.o.) for 25 days to the animals that were given rotenone. Behavioral experiment, i.e. cylinder test, was performed to assess the motor asymmetry. Animals were euthanized, and mid brains were isolated for the estimation of tricarboxylic acid cycle enzymes, oxidative measures (lipid peroxidation (LPO), glutathione (GSH) and catalase) and complex-I activity. In addition, histopathological studies were conducted. Fisetin treatment improved motor function in the cylinder test and reversed the rotenone-induced changes in mitochondrial enzymes, striatal dopamine levels, antioxidant enzyme levels and histological changes. An important finding of this study was both the doses of fisetin significantly (p < 0.05) enhanced rotenone-induced behavioral and biochemical changes and the effects were found to be dose dependent. Based on the present results, we hypothesize that fisetin may improve the mitochondrial enzyme activity, thereby preventing the pathogenesis of PD.
Insights
Fisetin treatment improved motor function and reversed Parkinson's disease (PD) symptoms in a rotenone-induced rat model. This natural compound may protect against PD by enhancing mitochondrial function.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Oxidative stress and mitochondrial complex-I inhibition are key in Parkinson's disease (PD) pathogenesis.
- Rotenone is a commonly used agent to induce a PD model in rodents.
- Fisetin is a natural flavonoid with potential antioxidant properties.
Purpose of the Study:
- To investigate the therapeutic potential of fisetin in a rotenone-induced rat model of Parkinson's disease.
- To evaluate the effects of fisetin on motor function, mitochondrial activity, oxidative stress markers, and neuroprotection.
Main Methods:
- Parkinson's disease was induced in rats using rotenone administration.
- Fisetin was administered orally at two different doses (10 mg/kg and 20 mg/kg).
- Behavioral tests (cylinder test), biochemical assays (TCA cycle enzymes, oxidative stress markers, complex-I activity), and histopathological examinations were performed.
Main Results:
- Fisetin treatment significantly improved motor function and reduced motor asymmetry in the cylinder test.
- Fisetin reversed rotenone-induced alterations in mitochondrial enzyme activity, striatal dopamine levels, and antioxidant status.
- Histopathological changes associated with rotenone-induced PD were ameliorated by fisetin treatment in a dose-dependent manner.
Conclusions:
- Fisetin demonstrates neuroprotective effects in the rotenone-induced rat model of Parkinson's disease.
- The findings suggest that fisetin may exert its beneficial effects by improving mitochondrial enzyme activity and combating oxidative stress.
- Fisetin holds promise as a potential therapeutic agent for Parkinson's disease.
