Journal
MEDIATORS OF INFLAMMATION
Volume 2017, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2017/2438247
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Background. Inflammation and fibrosis are the important pathophysiologic processes in diabetic nephropathy (DN). Maresin 1 is a potential anti-inflammatory lipid mediator, which has displayed powerful proresolving activities. Aim. We determine whether maresin 1 has protective effect on mouse glomerular mesangial cells (GMCs) induced by high glucose. Methods. We cultured GMCs stimulated by high glucose and categorized as follows: normal glucose group (5.6 mmol/L), high glucose group (30 mmol/L), mannitol group, maresin 1 intervention group (1, 10, and 100 nmol/L), maresin 1 and normal glucose group, and the N-acetylcysteine (NAC) intervention group (10 mu mol/LNAC). After 24 h, the expression of ROS, NLRP3, caspase-1, procaspase-1, IL-1 beta, and pro-IL-1 beta was detected by western-blot, RT-PCR, and immunofluorescence. After 48 h, the expression of TGF-beta 1 and FN was detected by RT-PCR and ELISA. Results. Compared with normal glucose group, the expression of ROS, NLRP3, caspase-1, IL-1 beta, TGF-beta 1, and FN increased in high glucose group (P < 0.05), but it decreased after the treatment of maresin 1 in different concentrations. On the contrary, the expression of procaspase-1 and pro-IL-1 beta protein was restrained by high glucose and enhanced by maresin 1 in a dose-dependent manner (P < 0.05). Conclusion. Maresin 1 can inhibit NLRP3 inflammasome, TGF-beta 1, and FN in GMCs; it may have protective effect on DN by mitigating the inflammation and early fibrosis.
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