title: [Effect of L-arginine on pulmonary surfactant and alveolar macrophages in rats with pulmonary injury induced by lipopolysaccharide].
abstract: OBJECTIVE
  To investigate the effect of L-Arginine (L-Arg) on pulmonary surfactant (PS) expression and alveolar macrophage (AM) in rats with pulmonary injury induced by lipopolysaccharide (LPS).
  
  
  METHODS
  Model of acute lung injury (ALI) was made by injection (iv) with LPS 5 mg/kg in rats. Fourty-eight male SD rats were randomly divided into 3 groups(n = 16): control, model (LPS) and L-Arg groups. L-Arg (500 mg/kg ip ,L-Arg group) or saline (control and LPS group) was administrated at 3 h or 6 h after LPS injection respectively for 3 h. The expression of surfactant protein A (SP-A) mRNA in the lung tissue was detected by ISH. The total protein (TP) in the bronchoalveolar lavage fluid (BALF) was detected. Rat AM were isolated from the bronchial alveolar lavage fluid of SD rats and harvested by selective plating technique. LPS and L-Arg were added to the culture medium. The concentration of nitric oxide (NO),the activity of lactate dehydrogenase (LDH), the contents of tumor necrosis factor alpha (TNF-alpha) and interleukin- 6 (IL-6) in the culture supernatants were respectively measured.
  
  
  RESULTS
  Compared with the control group, the expression of SP-A mRNA was significantly decreased, the TP concentration was significantly increased in LPS group. Compared with LPS group at the same time points, treatment with L-Arg at 3 h after LPS, the expression of SP-A mRNA in lung tissue was increased markedly, whereas TP concentration was decreased significantly. In cultured rat AM, LDH activity, NO, TNF-alpha and IL-6 contents in culture medium were significantly increased in LPS group to compared with those of control group. LDH activity, TNF-alpha and IL-6 contents were decreased in L-Arg group compared with those of LPS group.
  
  
  CONCLUSIONS
  L-Arg can protect the lung against LPS-induced pulmonary injury by up-regulating the expression of PS and inhibiting inflammatory transmitters from AM.
authors.affiliation: Institute of Materia Medica, Hebei Provincial Centre for Disease Prevention and Control, Shijiazhuang, China.
authors.forename: Li-ping
authors.initials: LP
authors.lastname: Li
authors.forename: Jian-xin
authors.initials: JX
authors.lastname: Zhang
authors.forename: Lan-fang
authors.initials: LF
authors.lastname: Li
authors.forename: Li-jun
authors.initials: LJ
authors.lastname: Xie
authors.forename: Qin-zeng
authors.initials: QZ
authors.lastname: Zhang
authors.forename: Na
authors.initials: N
authors.lastname: Hao
authors.forename: Guo-feng
authors.initials: GF
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D000818:Animals; D001120:Arginine / Q000494:pharmacology* / Q000627:therapeutic use; D008070:Lipopolysaccharides / Q000009:adverse effects; D016676:Macrophages, Alveolar / Q000378:metabolism*; D008297:Male; D011663:Pulmonary Surfactants / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D008070:Lipopolysaccharides; D011663:Pulmonary Surfactants; D001120:Arginine