Benzodiazepines, such as Valium and Xanax, are commonly prescribed to treat anxiety, insomnia, and seizures.
While these drugs can be helpful in the short term, long-term use has been linked to troubling side effects, including increased risk of inflammation and conditions like lung disease and inflammatory bowel disease.
For years, scientists have struggled to understand exactly why these side effects happen. Now, new research may finally have an answer.
A study led by scientists at Virginia Commonwealth University and Columbia University has uncovered important details about a protein in the body called HsTSPO1, which could be the missing link in understanding the side effects of benzodiazepines.
The findings, recently published in The Proceedings of the National Academy of Sciences, may not only help improve benzodiazepine drug design, but could also lead to new treatments for inflammation-related diseases like Alzheimer’s, arthritis, certain cancers, and multiple sclerosis.
Benzodiazepines work by calming the brain through their interaction with GABAA receptors. But they also bind strongly to HsTSPO1, a protein found on the surface of mitochondria—tiny energy-producing parts of cells.
HsTSPO1 has long been suspected to play a role in how these drugs affect the body beyond the brain, but its exact structure and function remained unclear, making it difficult for researchers to confirm its role or target it effectively with drugs.
To crack the case, the research team developed a new method for studying proteins without the use of harsh detergents, which often damage delicate cell structures.
Instead, they used a “native membrane nanoparticle” system that preserves the protein in a state much closer to how it exists in the body.
This allowed them to get a better look at how HsTSPO1 behaves under natural conditions.
Their discovery was surprising and exciting. They found that HsTSPO1 behaves like an enzyme, breaking down a compound called protoporphyrin IX—which is found in red blood cells—to create a newly discovered molecule named bilindigin.
This molecule appears to help control the levels of reactive oxygen species (ROS), which are unstable molecules that can damage cells and cause inflammation if not properly regulated.
The researchers now believe that when benzodiazepines bind to HsTSPO1, they may block the protein’s ability to regulate ROS. This disruption could explain why long-term use of these drugs might increase the risk of inflammatory diseases.
Importantly, this research opens the door to developing better versions of benzodiazepines that don’t interfere with HsTSPO1’s activity. It also suggests that HsTSPO1 could become a valuable target for treating a range of diseases where inflammation and ROS play a key role.
According to lead researcher Dr. Youzhong Guo, this breakthrough could change the way we approach drug development—not only for anxiety medications but also for conditions like Alzheimer’s and arthritis.
As we continue to learn more about HsTSPO1, scientists hope to create safer, more effective treatments with fewer side effects.
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Source: Virginia Commonwealth University.
