Sesame oil waste seen to prevent Parkinson’s disease in mice

the study, “Sesaminol prevents Parkinson’s disease by activating the Nrf2-ARE signaling pathway, ”Was published in the journal helix..

Parkinson’s disease is characterized by the loss of neurons that produce dopamine, a chemical required for a variety of behaviors, from muscle control and coordination to cognitive function.

Current treatments can relieve the symptoms of Parkinson’s disease, but they cannot stop the progression of the disorder. What may be an important research priority.

Researchers at Osaka City University in Japan suggest that a good candidate for such a drug is sesaminol, a chemical found in sesame shells. After extracting sesame oil from the seeds, empty husks are generally discarded as waste.

In a series of experiments, Dr. Akiko Kojima and her colleagues found that sesaminol prevented nerve damage and the appearance of some Parkinson’s disease symptoms in a mouse model of the disease.

The team first tested the neuroprotective effect of sesaminol on cell culture. They mimicked the cellular effects of Parkinson’s disease by treating human neurons with 6-OHDA, a neurotoxin used to selectively destroy dopaminergic neurons.

One way 6-OHDA damages these neurons is to cause an increase in reactive oxygen species (ROS), which are chemically reactive oxygen species that create a harsh cellular environment commonly known as oxidative stress. is.

Nerve cells treated with sesaminol 2 hours prior to 6-OHDA introduction were less damaged and less likely to die than untreated cells.

Researchers also observed that in sesaminol-treated cells, a protein called Nrf2 migrates to the nucleus, producing antioxidants and reducing ROS production, allowing cells to resist oxidative stress. Did.

To investigate what these cellular effects mean in living animals, researchers initiated Parkinson’s disease-like syndrome in mice by treating them with the insecticide / insecticide rotenone. ..

Mice given rotenone showed movement disorders such as imbalance of rotating rods, whereas mice given rotenone and sesaminol functioned similarly to control mice that were not given either chemical. ..

Mice fed sesaminol had less loss of dopaminergic neurons and less accumulation of Lewy bodies, a toxic mass of α-synuclein common to Parkinson’s disease, compared to mice fed rotenone alone. It was.

Sesaminol treatment also prevented some Parkinson-related gastrointestinal problems common to patients.

People with Parkinson’s disease often experience constipation, essentially a slowdown in the gastrointestinal system. Mice given rotenone had constipation, but mice given sesaminol did not.

Finally, mice fed sesaminol showed no signs of damage to the lamina propria of the intestine, the protective barrier that lines the intestine. Damage to this layer, Including presence Lewy body dementias has been recorded in Parkinson’s disease.

“These results show that sesaminol is very suitable for use as a prophylactic treatment. [Parkinson’s]The researchers concluded. “Practical application requires a more detailed elucidation of the mechanism of action.”

Yuasa Kojima is currently interested in extending the work of the team to clinical trials.As she explained in college Press releaseBy using food waste as a medicine, we can link production and consumption in a way that “prevents diseases caused by natural foods and greatly promotes social health.”

Forest Ray holds a PhD in Systems Biology from Columbia University and has developed tools to adapt the side effects of drugs to other diseases. Since then, he has worked as a journalist and science writer, covering topics from rare diseases to the crossroads of environmental science and social justice. He currently lives in Long Beach, California.

Total number of posts: 208

Ana holds a PhD in immunology from the University of Lisbon and worked as a postdoctoral fellow at the Instituto de Medicina Molecular (iMM) in Lisbon, Portugal. She holds a Bachelor of Science degree in Genetics from Newcastle University and a Master’s degree in Biomolecular Archeology from the University of Manchester, England. After leaving the lab to pursue a science communication career, she was the director of science communication at iMM.

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