Arbutin, a natural compound found in plants such as bearberry leaves and pear trees, was able to protect dopaminergic neurons and reduce behavioral deficits and oxidative stress in an animal model of Parkinson’s disease, a study reports.
The study, “Arbutin attenuates behavioral impairment and oxidative stress in an animal model of Parkinson’s disease,” was published in the Avicenna Journal of Phytomedicine.
Parkinson’s disease is characterized by the progressive deterioration and death of a specific subset of brain cells called dopaminergic neurons. The loss of these nerve cells causes the disease’s neurological symptoms such as tremors, muscle rigidity, slow movements, and postural instability.
However, the molecular mechanisms by which these dopaminergic neurons are selectively affected and degenerate over time remains unknown.
Increasing evidence shows that oxidative stress is an important factor that contributes to disease progression.
Oxidative stress is caused by an imbalance between the body’s production of potentially harmful reactive oxygen species and the ability of cells to detoxify them. These reactive oxygen species can damage crucial molecules in cells including DNA and proteins, hampering their function and ultimately their ability to survive.
Current treatment options for Parkinson’s are still limited, losing effectiveness over time and often associated with side effects including nausea, fatigue, fainting, and increased tremors. Therefore, new therapeutics are urgently needed.
In this study, researchers investigated the effectiveness of a new compound — arbutin — in the treatment of Parkinson’s disease. Arbutin is naturally found in various plants, such as bearberry leaves and pear trees.
The team used a mouse model that mimics the symptoms and molecular alterations of the human disease. Mice were injected with 1-methyl-4-phenyl- 1,2,3,6-tetrahydropyridine (MPTP), known for inducing Parkinson’s symptoms similar to those observed in human patients.
Animals were divided into three groups — a control group injected with a saline (innocuous) solution; a second group treated with a saline solution for seven days, followed by MPTP, injected into the abdomen; and a third group receiving arbutin (50 mg/kg) injected into the abdomen, before receiving MPTP injections.
On the 14th day of the experiment, researchers evaluated behavioral deficits using a locomotion test, hanging wire test, and forepaw stride length. They also analyzed the animals’ blood and brain tissue.
Arbutin-treated animals improved their locomotor activity and increased their forepaw step distance over the controls. Treated animals were also able to hand upside down (hanging wire test) for longer periods of time than the controls.
Arbutin also reduced blood and brain levels of specific molecules associated with oxidative stress, such as nitric oxide, previously shown to promote the death of dopaminergic neurons. The expression of thiobarbituric acid reactive substance (TBARS), a marker of oxidative stress whose levels were reported to be higher in the brains of Parkinson’s patients, was also reduced, both in the brain and blood of arbutin-treated animals.
These findings suggest that “arbutin can effectively attenuate behavioral deficits and reduce oxidative and nitrosative stress in MPTP- induced PD [Parkinson’s] model,” the researchers wrote.
They are now interested in clarifying “the exact molecular mechanisms by which arbutin can protect dopaminergic neurons.”
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