Troglitazone-activated PPARγ inhibits LPS-induced lung alveolar type II epithelial cells injuries via TNF-α.
Acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) are common syndromes characterized by diffuse, acute injury to the alveolar epithelium and pulmonary vascular endothelial cells, with high mortality rate for there are no effective pharmacological therapies. Peroxisome proliferators-activated receptor γ (PPARγ), a member of the nuclear hormone receptor superfamily of ligand-activated transcription factors, is ubiquitously expressed within the lung. Recent studies have indicated PPARγ can protect lung tissue and alleviate pulmonary inflammatory injury. But no studies examined whether PPARγ agonists can protect the alveolar epithelial cells cultured in vitro. We observed the protective effect of PPARγ in LPS-induced alveolar type II epithelial cells injury. The results showed troglitazone-activated PPARγ could inhibit the production of TNF-α, one of the most important inflammatory factors, and then increased the expression of surfactant-associated protein A (SP-A) and attenuate the apoptosis of alveolar type II epithelial cells. Our results suggest that PPARγ may have a potential therapeutic effect on ALI.
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