Chinese Herbal Remedy Prevents Healthy Airway Cells from Transitioning to Fibrotic Ones, Study Shows
A Chinese herbal remedy prevented healthy airway surface cells from transitioning to the type of cells seen in pulmonary fibrosis, a study reported.
It did this by inhibiting the body’s production of proteins involved in fibrosis, or scarring, including HMGB1, TLR-4, and HIF-1α.
The results prompted researchers to suggest that the remedy, known as pulmonary rehabilitation mixture, or PHM, could be used to treat lung fibrosis. The herbal mixture is also known as Fei-Fu-Kang.
The study, “Pharmacodynamic and pharmacokinetic assessment of pulmonary rehabilitation mixture for the treatment of pulmonary fibrosis,” was published in the journal Scientific Reports.
PRM is a mixture of seven herbs containing compounds with medicinal qualities. Although studies have suggested that the traditional mixture benefited animal models of lung fibrosis, no study had mapped how it affects disease processes.
A Binzhou Medical University team decided to look at the mixture’s pharmacokinetics, or how the body processes the compounds.
Researchers started with lab-grown cells exposed to the fibrosis trigger cobalt chloride. They discovered that PRM prevented healthy airway surface cells from transitioning to the type of cells seen in fibrotic airways — a process called epithelial to mesenchymal transition. They saw the same thing when they studied cells that line blood vessels.
The remedy may work by reducing production of proteins involved in disease processes, including HMGB1, TLR-4 and HIF-1α, the team said.
They next studied the processes in a rat model of pulmonary fibrosis. Just as they observed in the lab-grown cells, PRM lowered a range of fibrosis-related proteins, including FGF-2, PDGF, TLR-4, HMGB1, and HIF-1α, the team said.
A hallmark of fibrosis is an increase in cells known as pulmonary fibroblasts, at the expense of other cells. PRM lowered the cells’ growth in rats.
Researchers detected five compounds from the herbal mixture in the rats’ blood, suggesting that the body absorbed the drug from the gut after it was ingested. The concentration of some of the compounds, and the time it took for them to be cleared from the body, differed between healthy and diseased rats. The reason needs to be studied, the team said.
Nonetheless, the team concluded that “PRM exhibited a satisfactory pharmacodynamic and pharmacokinetic performance which highlights PRM as a potential multi-target oral drug for the treatment of pulmonary fibrosis.”