• C Yi, S R Wang, S Y Zhang, S J Yu, C X Jiang, M H Zhi, and Y Huang.
• Cancer Center, Huaxi Hospital, Sichuan University, Chengdu, 610041, Sichuan Province, China. yicheng6834@163.com
• Inflamm. Res. 2006 Nov 1; 55 (11): 491-7.

ObjectiveTo investigate the effects of recombinant human growth hormone (rhGH) on rat acute lung injury (ALI).MethodsALI was mimicked by intraperitoneal (i. p.) injection of E. coli. Female Sprague-Dawley rats were randomized into three groups: control group, injected with physiologic saline (i. p.); ALI group, received a bolus injection of E. coli (1 x 10(10) cfu/l, 15 ml/kg, i. p.) followed by intramuscular physiologic saline injection; and ALI + GH group, received a bolus administration of E. coli, and then treated with intramuscular rhGH injection (2.25 U/kg/d). ALI group and ALI + GH group were subdivided into day 1 and day 3 subgroups, respectively. Left lungs were lavaged and bronchial alveolar lavage fluid (BALF) was harvested. Lung injury score, lung wet-to-dry weight (W/D) ratio, percentage of neutrophils (PMNs) in BALF, lung permeability index (LPI), intercellular adhesion molecule-1(ICAM-1) expression and activation of nuclear factor-kappa B (NF-kappaB) in the lungs were determined.Results(1) On day 1 and day 3, the lung injury score, lung W/D ratio, LPI and protein content in BALF were significantly higher in the ALI group than in the control and ALI + GH groups. rhGH attenuated lung injuries significantly. (2) Compared with the control group, the percentage of PMNs in BALF was elevated significantly in the ALI and ALI + GH groups, especially in ALI group. (3) Nuclear positive rate of NF-kappaB and ICAM-1 expression at the levels of protein and mRNA in the lung in the ALI group on day 1 and day 3 were higher than in the control group. rhGH diminished activation of NF-kappaB and expression of ICAM-1 in the lung markedly.ConclusionsTreatment with rhGH can significantly attenuate lung injury in the endotoxemic rats, which may be attributed to the reduction of the expression of ICAM-1, the influence on the adhesion and activation of PMNs, the inhibition of the activation of NF-kappaB and the regulation of the transcription of certain proinflammatory cytokines.

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