[High-density lipoprotein attenuates lipopolysaccharide-induced acute lung injury in mice].
High-density lipoprotein (HDL), an abundant plasma lipoprotein, has been thought to be anti-inflammatory in both health and infectious diseases. It binds lipopolysaccharide (LPS) and neutralizes its bioactivity. The present study aimed to investigate the potential role of HDL, which was separated from human plasma, in LPS-induced acute lung injury in mice. Kunming mice (18-22 g) were treated with either HDL (70 mg/kg body weight, via tail vein) or saline 30 min after LPS administration (10 mg/kg body weight, intraperitoneally) and were decapitated 6 h after LPS challenge. The arterial blood was collected and analyzed for blood gas variables (PaO(2), pH, and PaCO(2)). The bronchoalveolar lavage fluid (BALF) samples were analyzed for total protein concentration, lactate dehydrogenase (LDH) activity, and white blood cell (WBC) count. The lung samples were taken for histopathological evaluation and for determination of lung wet-to-dry weight ratio (W/D), malondialdehyde (MDA) content, myeloperoxidase (MPO) activity and tumor necrosis factor α (TNF-α) content. Arterial blood gas analysis showed that after LPS challenge, HDL-treated mice exhibited a higher PaO(2), and pH, but a lower PaCO(2) than HDL-untreated ones (P<0.01). LPS-induced increases in total protein concentration, WBC number and LDH activity in BALF were significantly attenuated in HDL-treated mice (P<0.01). HDL treatment also resulted in a significant protection of lung tissues against LPS-induced acute lung injury via decreasing W/D ratio, MPO activity, MDA content, and the content of the pro-inflammatory cytokine TNF-α (P<0.05, P<0.01). Histological examination revealed that HDL treatment resulted in significantly lower scores of acute lung injury induced by LPS, with reduced hemorrhage, intra-alveolar edema and neutrophilic infiltration (P<0.01). It is suggested that HDL plays a protective role in attenuating LPS-induced acute lung injury in mice.
Grade 2004, Xiangya School of Medicine, Central South University, Changsha 410078, China.
Ge-Lei
GL
Xiao
Zi-Qiang
ZQ
Luo
Gong
G
Xiao
Chen
C
Li
Xu-Dong
XD
Xiong
Ying
Y
Yang
Hui-Jun
HJ
Liu
D055371:Acute Lung Injury / Q000139:chemically induced / Q000628:therapy*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D007249:Inflammation / Q000378:metabolism; D007958:Leukocyte Count; D008070:Lipopolysaccharides / Q000009:adverse effects; D008075:Lipoproteins, HDL / Q000494:pharmacology*; D008168:Lung / Q000473:pathology*; D008315:Malondialdehyde / Q000378:metabolism; D051379:Mice; D009195:Peroxidase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde; D009195:Peroxidase