Sesaminol, a waste product of sesame oil production with antioxidant properties that might protect nerve cells, was found to prevent some symptoms of Parkinson’s disease in a mouse model in a recent study.
Treated mice, its researchers reported, showed better balance and fewer gastrointestinal issues than mice in this model not fed sesaminol.
The study, “Sesaminol prevents Parkinson’s disease by activating the Nrf2-ARE signaling pathway,” was published in the journal Heliyon.
Parkinson’s disease is characterized by the loss of neurons that produce dopamine, a chemical needed for a range of behaviors, from muscle control and coordination, to cognitive functions.
Current therapies can ease some Parkinson’s symptoms, but cannot stop the disorder’s progression. Those that might are a key research priority.
Researchers with Osaka City University, in Japan, suggest a good candidate for such a medication is sesaminol, a chemical found in sesame seed shells. After sesame oil is extracted from the seeds, the empty shells are generally discarded as waste.
In a series of experiments, Akiko Kojima-Yuasa, PhD, and her colleagues found that sesaminol prevented nerve damage and the emergence of some Parkinson’s symptoms in a mouse model of the disease.
The team first tested sesaminol’s neuroprotective effects in cell cultures. They mimicked Parkinson’s cellular effects by treating human nerve cells with 6-OHDA, a neurotoxin used to selectively destroy dopamine-producing neurons.
One way in which 6-OHDA causes damages these neurons is by triggering an increase in reactive oxygen species (ROS), chemically reactive forms of oxygen that create harsh cellular environments broadly known as oxidative stress.
Nerve cells treated with sesaminol two hours prior to 6-OHDA’s introduction showed less damage and were less likely to die than their untreated counterparts.
Researchers also observed that within sesaminol-treated cells, a protein called Nrf2 migrated to the nucleus, where it enabled cells to resist oxidative stress by producing antioxidants and lowering ROS production.
To investigate what these cellular effects might mean in a living animal, the investigators initiated a Parkinson’s-like syndrome in mice by treating them with the insecticide/pesticide rotenone.
While mice fed rotenone showed motor deficits, such as losing balance on a rotating rod, those fed rotenone and sesaminol performed as well as the control mice, who were fed neither chemical.
Compared to mice fed only rotenone, those also fed sesaminol lost fewer dopamine-producing neurons, and accumulated fewer Lewy bodies — toxic clumps of alpha-synuclein common to Parkinson’s.
Sesaminol treatment also prevented several Parkinson’s-related gastrointestinal problems common to patients.
People with Parkinson’s often experience constipation, essentially a slowdown of the gastrointestinal system. While mice fed rotenone had constipation, those also fed sesaminol did not.
Finally, sesaminol-fed mice showed no sign of damage to the intestinal mucosal layer, a protective barrier lining the inside of the intestines. Damage to this layer, including the presence of Lewy bodies, has been documented in Parkinson’s.
“These results show that sesaminol is very suitable for use as a preventive treatment of [Parkinson’s],” the researchers concluded. “Further detailed elucidation of the mechanism of action will be necessary for practical application.”
Kojima-Yuasa is now interested in extending her team’s work to clinical trials. As she explained in a university press release, the use of food waste as medicine can connect production and consumption in a way that “prevents diseases with natural foods to greatly promote societal health.”
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