某抗氧化药物可抑制鼠类多发性硬化

Researchers at Oregon Health & Science University have discovered that an antioxidant designed by scientists more than a dozen years ago to fight damage within human cells significantly helps symptoms in mice that have a multiple sclerosis-like disease. The antioxidant -- called MitoQ -- has shown some promise in fighting neurodegenerative（神经变性的） diseases. But this is the first time it has been shown to significantly reverse an MS-like disease in an animal.

 

The discovery could lead to an entirely¹ new way to treat multiple sclerosis（多发性硬化）, which affects more than 2.3 million people worldwide.

 

Multiple sclerosis occurs when the body's immune system attacks the myelin（髓磷脂）, or the protective sheath（接地屏蔽）, surrounding nerve fibers² of the central nervous system. Some underlying³ nerve fibers are destroyed. Resulting symptoms can include blurred⁴ vision and blindness, loss of balance, slurred⁵ speech（口齿不清）, tremors⁶, numbness⁷ and problems with memory and concentration.

 

The antioxidant research was published in the December edition of Biochimica et Biophysica Acta Molecular⁸ Basis of Disease. The research team was led by P. Hemachandra Reddy, Ph.D., an associate scientist in the Division of Neuroscience at OHSU's Oregon National Primate⁹ Research Center.

 

To conduct their study, the researchers induced mice to contract a disease called experimental autoimmune encephalomyelitis（脑脊髓炎）, or EAE, which is very similar to MS in humans. They separated mice into four groups: a group with EAE only; a group that was given the EAE, then treated with the MitoQ; a third group that was given the MitoQ first, then given the EAE; and a fourth "control" group of mice without EAE and without any other treatment.

 

After 14 days, the EAE mice that had been treated with the MitoQ exhibited reduced inflammatory markers and increased neuronal activity in the spinal¹⁰ cord -- an affected¹¹ brain region in MS -- that showed their EAE symptoms were being improved by the treatment. The mice also showed reduced loss of axons, or nerve fibers and reduced neurological disabilities associated with the EAE. The mice that had been pre-treated with the MitoQ showed the least problems. The mice that had been treated with MitoQ after EAE also showed many fewer problems than mice who were just induced to get the EAE and then given no treatment.

 

"The MitoQ also significantly reduced inflammation of the neurons and reduced demyelination," Reddy said. "These results are really exciting. This could be a new front in the fight against MS."

 

Even if the treatment continues to show promise, testing in humans would be years away. The next steps for Reddy's team will be to understand the mechanisms¹² of MitoQ neuroprotection in different regions of the brain, and how MitoQ protects mitochondria within the brain cells of the EAE mice. Mitochondria, components¹³ within all human cells, convert energy into forms that are usable by the cell.

 

There is a built-in advantage with MitoQ. Unlike many new drugs, MitoQ has been tested for safety in numerous clinical trails with humans. Since its development in the late 1990s, researchers have tested MitoQ's ability to decrease oxidative damage in mitochondria.

 

"It appears that MitoQ enters neuronal mitochondria quickly, scavenges free radicals¹⁴, reduces oxidative insults produced by elevated inflammation, and maintains or even boosts neuronal energy in affected cells," said Reddy. The hope has been that MitoQ might help treat neurodegenerative diseases like Alzheimer's and Parkinson's. Studies evaluating its helpfulness in treating those diseases are ongoing¹⁵.

分享到：