Blocking sodium sensor Nax with a nanoparticle-carried RNAi may eventually provide novel treatments for wounds and burns. [iStock/Pamela Moore]
Blocking sodium sensor Nax with a nanoparticle-carried RNAi may eventually provide novel treatments for wounds and burns. [iStock/Pamela Moore]

Researchers at Louisiana State University along with collaborators at Northwestern University say they have discovered a new way to prevent inflammation and to accelerate the skin's healing process. After five years of research, they identified the gene regulation pathway, which involves the body's sodium sensor called Nax (scn7a) that triggers inflammation. They found a way to block it using a nanoparticle-carried small interference RNA, which enables the skin to heal faster.

“This is a really novel pathway we identified. Nobody has ever tried to develop a product that gets at this pathway before,” said Wei Xu, Ph.D., assistant professor at the LSU AgCenter and the School of Renewable Natural Resources.

Dr. Xu and his team developed a nanoparticle which delivers the RNA that inhibits Nax, thus preventing inflammation. The nanoparticle can be applied to the skin in a cream or lotion. Their study, entitled “Sodium channel Nax is a regulator in epithelial sodium homeostasis research”, appears in Science Translational Medicine.

“I think this is going to be very promising in skin disease treatments,” Xu said.

This discovery was built upon previous work that showed areas of skin with high hydration heal faster. Combined with the fact that human skin holds more than 100 times as much sodium than most other ions, this led the researchers to believe that the body's sodium regulators were key components. One sodium channel, Nax, is particularly sensitive to the body's changes in salt concentration. Moreover, Nax had already been shown to also regulate sodium levels in the central nervous system.

Dr. Xu applied the DNA microarray technique to screen more than 100,000 genes in the human genome to find the exact gene regulation pathway.

“If we target the very beginning of the pathway, we can control the expression levels of the inflammation factors,” he explained.








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