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Offering hope of potential therapies for people suffering from diseases such as rheumatoid arthritis, osteoarthritis and asthma, researchers at the University of California, Davis, have demonstrated in studies with mice that a particular chemical compound plays a critical role in the inflammation process.

Findings from the study, conducted by entomology professor Bruce Hammock and colleagues, are reported online in this week's issue of the journal Proceedings of the National Academy of Sciences.

"As of 2004, anti-inflammatory medications were being prescribed for more than 73 million people, yet many continued to suffer from these diseases or side effects of the medicines," said Hammock. "We are hopeful that this study will bring us one step closer to development of safe and effective treatments for the inflammatory process that is so key to these diseases."

In an earlier study, Hammock, doctoral candidate Kara Schmelzer and colleagues identified a group of enzymes called sEH (soluble epoxide hydrolases), which break down anti-inflammatory compounds called epoxyeicosatrienoic acids (EETs). That study showed that rats injected with an sEH inhibitor experienced significantly less inflammation caused by exposure to tobacco smoke.

In the study reported this week, the researchers suspected that if they inhibited sEH in mice, blood levels of EETs would increase and inflammation would decrease. They first induced inflammation in both the test group and control group of mice, then treated the test group of mice with an sEH inhibitor.

The control group of mice, which had not received the sEH inhibitor, developed severe low blood pressure and died within four days.

The mice that had received the sEH inhibitor experienced a decrease in blood levels of the compounds that promote inflammation and an increase in the blood levels of EETs, which help resolve inflammation.

The results suggest that the sEH inhibitors might be useful in developing medicines for treating inflammatory diseases.

The researchers note that further studies are needed to explore the role of sEH in the inflammation process and to clarify how the sEH inhibitors work at the molecular level.

This research was supported by the National Institutes of Environmental Health Sciences, the Superfund Basic Research Program, the Center for Children's Environmental Health and Disease Prevention, and the University of California.