Journal of complementary & integrative medicine · 2026
Unveiling the mysteries: neuroprotective potential of Mucuna monosperma seeds in combating haloperidol induced Parkinsonism.
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Bhong Prabha, Ingale Suvarna, Jadhav Pallavi
Аннотация
OBJECTIVES: Parkinson's Disease (PD) is a progressive neurodegenerative disorder characterized by motor dysfunction and loss of dopaminergic neurons. Oxidative stress, defined as detrimental imbalance between free radicals and body's defense mechanism, is a critical contributing factor. This study evaluated the neuroprotective and antioxidant properties of methanolic extract of Mucuna monosperma seeds (MMMS) in haloperidol induced rat model of PD.
METHODS: PD was induced in rats by intraperitoneal administration of haloperidol (HPD, D2 blocker) at 1 mg/kg for 21 days. MMMS was administered orally at 100, 200, and 400 mg/kg. Motor abilities were assessed using the catalepsy bar test, actophotometer test, and rotarod test. Biochemical assessments measured markers of oxidative stress, and brain dopamine levels. Histopathological analysis was used to evaluate neuronal integrity.
RESULTS: Motor abilities were tested weekly for 21 days, followed by biochemical and histological analysis. HPD caused motor deficits, raised oxidative stress, and lowered dopamine. MMMS (400 mg/kg) improved motor function by decreasing catalepsy, increasing locomotion, and prolonging rotarod time (p < 0.0001). It also reduced oxidative stress, nearly normalized dopamine. Also, the levels of endogenous antioxidants like glutathione (GSH), super oxide dismutase (SOD), catalase (CAT) are also boosted and reduction of malonaldehyde (MDA), indicator of lipid peroxidation which may help in prevention of degradation of dopaminergic neurons. Histology showed better neuron preservation in MMMS rats.
CONCLUSIONS: This study found MMMS is neuroprotective in HPD-induced PD. Its effects likely stem from antioxidant properties, and dopamine restoration. MMMS may merit further research for PD management.
METHODS: PD was induced in rats by intraperitoneal administration of haloperidol (HPD, D2 blocker) at 1 mg/kg for 21 days. MMMS was administered orally at 100, 200, and 400 mg/kg. Motor abilities were assessed using the catalepsy bar test, actophotometer test, and rotarod test. Biochemical assessments measured markers of oxidative stress, and brain dopamine levels. Histopathological analysis was used to evaluate neuronal integrity.
RESULTS: Motor abilities were tested weekly for 21 days, followed by biochemical and histological analysis. HPD caused motor deficits, raised oxidative stress, and lowered dopamine. MMMS (400 mg/kg) improved motor function by decreasing catalepsy, increasing locomotion, and prolonging rotarod time (p < 0.0001). It also reduced oxidative stress, nearly normalized dopamine. Also, the levels of endogenous antioxidants like glutathione (GSH), super oxide dismutase (SOD), catalase (CAT) are also boosted and reduction of malonaldehyde (MDA), indicator of lipid peroxidation which may help in prevention of degradation of dopaminergic neurons. Histology showed better neuron preservation in MMMS rats.
CONCLUSIONS: This study found MMMS is neuroprotective in HPD-induced PD. Its effects likely stem from antioxidant properties, and dopamine restoration. MMMS may merit further research for PD management.