Mannose Prevents Acute Lung Injury Through Mannose Receptor Pathway And Contributes To Regulate Ppar. And Tgf-Beta 1 Level

Mannose has been reported to prevent acute lung injury (ALI), and mannose receptor (MR) has been demonstrated to have a role. The rationale for this study is to characterize the mechanism by which mannose and MR prevent lipopolysaccharide (LPS)-induced ALI. Male ICR mice were pretreated mannose by intravenous injection 5 min before and 3 h after intratracheal instillation of LPS. Pathological changes, proinflammatory mediator, peroxisome proliferator activated receptor gamma (PPAR gamma), MR, and transforming growth factor beta 1 (TGF-beta 1) levels were determined. The RAW264.7 cells were pretreated with mannose and stimulated with LPS for 3 h. Proinflammatory mediator and TGF-beta 1 in the culture media, PPAR gamma, MR, and TGF-beta 1 expression in RAW 264.7 cells were measured. Mannose markedly attenuated the LPS-induced histological alterations and inhibited the production of proinflammatory mediator in mice and in RAW 264.7 cells. Mannose increased PPAR gamma, and MR expression, and inhibited TGF-beta 1 stimulated by LPS. Interestingly, competitive inhibition of MR with mannan was associated with elimination of the anti-inflammatory effects of mannose, and reversed effects of mannose of regulation to PPAR gamma and TGF-beta 1. MR is important in increasing PPAR gamma and decreasing TGF-beta 1 expression and plays a critical role in mannose's protection against ALI.