Dipyrithione attenuates oleic acid-induced acute lung injury.
Dipyrithione (PTS2) has been shown to possess anti-bacterial and anti-fungal activities. Our previous study indicated that PTS2 inhibited iNOS and COX-2 up-regulation in response to LPS in RAW264.7 cells and protects mice against endotoxic shock. In the present study we observed effects of PTS2 on mouse acute lung injury (ALI) model induced by oleic acid (OA) to analyze the anti-inflammatory activities of PTS2 further. The morphological results showed that the OA induced a marked lung injury and this symptom was attenuated by PTS2. Furthermore, treatment mice with PTS2 significantly alleviated OA-induced microvascular leakage, and augment of MPO activity in lung tissue and level of IL-1β in BALF. Immunohistochemical observion displayed that PTS2 inhibited OA-induced enhanced expression of VCAM-1 and ICAM-1 in lung tissue. These findings suggest that PTS2 attenuates lung inflammation and suppresses OA-induced acute lung injury in mice.
Huang
Huang
H
State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, PR China.
Pan
Yu
Y
Ye
Yin
Y
Gao
Min
M
Yin
Zhimin
Z
Luo
Lan
L
D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy*; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D053583:Interleukin-1beta / Q000032:analysis; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D019301:Oleic Acid / Q000633:toxicity*; D009195:Peroxidase / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics
D053583:Interleukin-1beta; D011725:Pyridines; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D019301:Oleic Acid; C032196:dipyrithione; D009195:Peroxidase