A natural compound called gentiopicroside effectively lowers inflammation and tissue scarring in a mouse model of pulmonary fibrosis (PF), say researchers at China’s Kunming Medical University.
Since the plant-derived compound targets both fibrotic and inflammatory processes, researchers suggested it may be an ideal drug candidate for lung fibrosis — particularly in light of gastrointestinal disorders, hepatic dysfunction and other side effects caused by currently approved treatments.
Earlier studies show that gentiopicroside, which can be isolated from several different plants, has several useful properties, including anti-inflammatory and smooth muscle-relaxing activity.
The Chinese study, “Gentiopicroside ameliorates bleomycin-induced pulmonary fibrosis in mice via inhibiting inflammatory and fibrotic process,” appeared in the journal Biochemical and Biophysical Research Communications.
Researchers exposed mice to the fibrosis-triggering chemical bleomycin. Data showed that gentiopicroside-treated mice had significantly less collagen deposited in their lungs after bleomycin than did untreated animals.
The team tested two doses of the compound — 2.5 mg/ kg weight and 10 mg/ kg weight — and found that the higher dose produced a more robust response. Assessment of lung tissue under a microscope also showed that the treatment reduced inflammatory and fibrotic lesions.
They also found fewer inflammatory cells in the lungs; lung alveoli had not been as extensively distorted as in control animals.
The team then tested if gentiopicroside had any effect on known inflammatory and fibrotic molecules, and saw that the treatment did lower levels of the inflammatory factors TNF-alpha and IL-1 beta, as well as those of the profibrotic molecule TGF-beta. Again, researchers noted that the higher dose was more effective.
Experiments in lab-grown cells confirmed that gentiopicroside also affected other inflammatory and fibrotic markers.
Since approved PF medications don’t completely prevent the disease from worsening, researchers argued that continuing to search for new treatments is crucial. Such studies must make use of new knowledge of disease processes driving PF.
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