Protective Effect Of PTS2 On Oleic Acid Induced Acute Lung Injury

Diprithione (PTS2) is one of alkaloid and PTO has been shown to posses anti-bacterial and anti-fungal activities. The fact PTS2 has been demonstrated to induce apoptosis of Hella cells provides the possiblity that PTS2 could inhibit cancer. 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.The aim: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 and discuss the possible mechanism.The methods:(1) Mouse acute lung injury model was induced by caudal intravenous administration of 0.3mg/kg of oleic acid; (2) Mice pre- or post-treated with PTS2 (1.25,2.5 and 5mg/kg body weight) intraperitoneally 30 min before or after OA treatment, administration of DEX (dexamethasone,2mg/kg) as positive control; (3) Morphological changes, pulmonary microvascular leakage, MPO activity, level of IL-1βand TNF-αexpression of VCAM-1 and ICAM-1.The results:(1) The morphological results showed that the OA induced a marked lung injury and this symptom was attenuated by PTS2; (2) Treatment mice with PTS2 significantly alleviated OA-induced microvascular leakage; (3) PTS2 inhibited augment of MPO activity in lung tissue; (4) PTS2 treated mice showed decreased level of IL-1βand TNF-αin BLAF; (5) Immunohistochemical observation displayed that PTS2 inhibited OA-induced enhanced expression of VCAM-1 and ICMA-1 in lung tissue.These findings suggest that PTS2 attenuates lung inflammation and suppresses OA-induced acute lung injury in mice.