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New research shows that statins may protect against the severe inflammation that can lead to airway scarring and COPD—the incurable pulmonary disorder usually caused by smoking and the third highest cause of death in the US after heart disease and cancer. The study is the first to show that statins protect against bronchial, or large airway, injury—a key route to acute COPD complications.

For the study, published in the European Respiratory Journal, scientists at the University of California, Davis, exposed rats to high concentrations of tobacco smoke for three days—long enough to trigger acute, damaging airway reactions. Some of the animals were pre-treated with statins for 10 days before the smoke exposure.

The pre-treatment protected them from acute inflammation that destroys the lining of airways and leads to such symptoms as cough and phlegm production—and eventually to COPD and persistent breathlessness.

The 10-day pre-treatment was essential, researchers say. Treatment only during smoke exposure did not have the same protective effect, suggesting that statins may be protective against smoke-induced lung injury and possibly COPD, and that the timing of treatment may be important.

The scientists have launched new studies to determine if statins will protect air passageways from long-term tobacco smoke exposure, which often leads to COPD, physical debilitation, and oxygen dependence.

Smoking-induced inflammation leads to cell death and abnormal transformation of epithelial cells that line the airways. Smoking destroys the cells’ ability to clear the airways of toxins and other harmful particles.

“Many aspects of COPD are irreversible,” says Amir A. Zeki, one of the co-leaders of the research. “Once the mucosal surface of airway passages is damaged by inflammation, it can scar and lose its essential protective function. This can lead to chronic symptoms, shortness of breath, cough, and phlegm production. But the message here is that there may be hope for some patients with COPD.”

The rats received treatment with simvastatin by injection, the effects of which specifically targeted the lungs, says Kent Pinkerton, a collaborator on the research who developed the COPD animal model used in the study. Pinkerton is a professor of pediatrics at UC Davis Health System, professor of anatomy, physiology and cell biology at the UC Davis School of Veterinary Medicine and director of the UC Davis Center for Health and Environment.

The mechanism underlying the statin effect on inflammation is unknown, but the research demonstrates that a 10-day treatment with statins led to a “dramatic reduction” in acute inflammation, Pinkerton says.

“If this strategy holds true for patients, they may not need to take the drugs for an extended period to receive benefits,” says Ben Davis, a scientist in the Center for Health and Environment and the study’s first author.

Source: UC Davis