Japanese scientists have designed artificial molecules that reversed liver cirrhosis in rats.

Cirrhosis is a hardening or scarring of the liver that occurs when liver cells begin producing collagen, a fibrous material found in skin and tendons.

The researchers said they designed molecules that block collagen production by the liver’s “stellate cells,” which are also known to absorb vitamin A. The scientists loaded these molecules into vitamin-A coated carriers, which tricked the stellate cells into absorbing the molecules.

“By packaging the (molecules) in carriers coated with vitamin A, they tricked the stellate cells into letting in the inhibitor, which shut down collagen secretion,” the researchers wrote in a report about their work.

During the study, the researchers injected the vitamin A-laced molecules in rats with induced liver cirrhosis.

“We were able to completely eradicate the fibrosis by injecting this agent … we cured them of the cirrhosis,” said Yoshiro Niitsu of Sapporo Medical University School of Medicine, during a telephone interview with Reuters.

“The liver is such an important organ, after you remove the fibrosis, the liver by itself starts to regenerate tissues. So liver damage is reversible,” he added.

“Liver is itself responsible for the production and deposition of collagen, it also secretes certain enzymes that dissolve collagen … dissolve the fibrosis which has already been deposited in the tissues,” Niitsu said, explaining the how the damage reversal came about.

Cirrhosis is often caused by Hepatitis B and C, or by heavy drinking, and is especially serious in parts of Asia. Until now, liver damage from cirrhosis was thought to be irreversible, and the disease cured only with transplants.

But Niitsu is optimistic that in time the molecules would provide a cure.

“We hope it (a drug) will be ready for humans in a few years,” he said.

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Sapporo Medical University School of Medicine

The research was published in the journal Nature Biotechnology. A summary can be viewed at http://www.nature.com/nbt/journal/vaop/ncurrent/abs/nbt1396.html

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