Seed extract restores dopamine in Parkinson’s rat model

An extract from the seeds of Mucuna monosperma, a flowering plant, protected nerve cells in the brain and restored dopamine in a rat model of Parkinson’s disease, a study has found.

However, more research is needed to determine whether it is safe and effective for patients. Dopamine is a chemical needed to control movement.

The extract may target Parkinson’s core disease-causing mechanism rather than just easing the disease’s symptoms, researchers noted in “Unveiling the mysteries: neuroprotective potential of Mucuna monosperma seeds in combating haloperidol induced Parkinsonism,” which was published in the Journal of Complementary and Integrative Medicine.

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Parkinson’s occurs due to the gradual damage to nerve cells that produce dopamine, a chemical in the brain that helps the body control movement. As dopamine-producing nerve cells are lost, patients can experience symptoms such as tremors, stiffness, and balance problems.

Mucuna monosperma is a species of flowering plant in the legume family, which includes beans and peas. In this study from India, the researchers prepared an extract from its seeds and tested its potential to protect against oxidative stress, an imbalance that occurs when harmful, reactive molecules overwhelm the body’s antioxidant defenses and cause cellular damage.

Chemical analysis showed that each gram of dry extract contained nearly 20 mg of L-DOPA, which the body can use to produce dopamine. L-DOPA is also known as levodopa, the gold standard for treating Parkinson’s. The researchers also detected active compounds with antioxidant properties, including flavonoids, phenolics, and tannins.

The extract was tested in a rat model that mimics Parkinson’s by injecting haloperidol for three weeks. Haloperidol blocks D2 receptors, which normally respond to dopamine. The rats received the extract orally daily at doses of 100 mg, 200 mg, or 400 mg/kg, alongside haloperidol. For comparison, the researchers included healthy rats, untreated rats, and rats treated with levodopa and carbidopa, which allows more levodopa to reach the brain.

[The extract’s] specific bioactive components and molecular targets have yet to be determined.

Motor symptoms were assessed using three tests: the catalepsy bar test, which measures muscle stiffness; the actophotometer test, which measures spontaneous movement; and the rotarod test, which assesses balance, coordination, and the ability to remain on a rotating rod. Tests were conducted weekly for three weeks, followed by microscopic examination of brain tissue.

Haloperidol-treated rats developed greater muscle stiffness than healthy rats. The extract reduced muscle stiffness in a dose-dependent manner, meaning higher doses generally produced greater improvements. The two higher doses also increased spontaneous movement and the time rats remained on the rotating rod.

When the researchers measured levels of antioxidant molecules, they found that the highest dose of the extract increased glutathione, which neutralizes toxic, unstable molecules. It also increased the levels of superoxide dismutase and catalase, two enzymes that help break down these molecules. Malondialdehyde, which indicates damage to fats in cell membranes caused by oxidation, was reduced.

Compared with untreated rats, rats treated with the extract had significantly higher dopamine levels in the brain. Microscopic examination of the midbrain, a region involved in movement control, showed that haloperidol caused severe damage to nerve cells and gliosis, an increase in supporting cells in response to damage. The extract reduced this damage, particularly at the highest dose tested.

Although the extract appears to protect against oxidative stress, “its specific bioactive components and molecular targets have yet to be determined,” the researchers wrote. “Future research should aim to isolate the active compounds, clarify the mechanisms involved, and explore the pharmacokinetic profile,” that is, how its compounds move into, through, and out of the body.