Effect of L-arginine on pulmonary surfactant in the rats with LPS-induced acute lung injury
Liping Li, Jianxin Zhang, Lanfang Li, Lijun Xie, Zhang Qin-zeng, Guofeng Li, Na Hao
Abstract
Liping Li, Jianxin Zhang, Lanfang Li, Lijun Xie, Zhang Qin-zeng, Guofeng Li, Na Hao
Abstract
Objectiye To investigate the effect of L-arginine on pulmonary surfactant (PS) in the rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods Forty-eight adult male SD rats weighing 220-270 g were randomly divided into 4 groups:group Ⅰ control (group C);group Ⅱ LPS;group Ⅲ LPS 3 h + L-arginine(group L1);group Ⅳ LPS6 h + L-arginine(group L2). ALI was induced by intravenous (Ⅳ)LPS 5 mg/kg in LPS,L1 and L2 groups. L-arginine 500 mg/kg was given intraperitoneally at 3 or 6 h after LPS administration in group L1 or group L2. The animals were sacrificed at 3 h after L-arginine administration, eight animals were sacrificed at 6 h and 9 h after LPS in group C and group LPS. The lungs were immediately removed for determination of surfactant-protein (SP-A) mRNA expression and broncho-alveolar lavage fluid (BALF). The total phospholipid (TPL) and total protein (TP) concentrations in the BALF were measured. Results SP-A mRNA in the lung tissue and TPL concentration in BALF were significantly decreased while TP concentration in BALF was significantly increased in group LPS, as compared with control groups( P < 0.01 ). L-arginine given at 3 h after LPS administration significantly attenuated the LPS-induced changes while L-arginine given at 6 h after LPS did not. Conclusion L-arginine can protect the lungs from LPS-induced injury by up-regulating PS-expression. Key words: Arginine; Endotoxemia; Respiratory distress syndrome, adult; Pulmonary surfactantassociated proteins
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Objectiye To investigate the effect of L-arginine on pulmonary surfactant (PS) in the rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods Forty-eight adult male SD rats weighing 220-270 g were randomly divided into 4 groups:group Ⅰ control (group C);group Ⅱ LPS;group Ⅲ LPS 3 h + L-arginine(group L1);group Ⅳ LPS6 h + L-arginine(group L2). ALI was induced by intravenous (Ⅳ)LPS 5 mg/kg in LPS,L1 and L2 groups. L-arginine 500 mg/kg was given intraperitoneally at 3 or 6 h after LPS administration in group L1 or group L2. The animals were sacrificed at 3 h after L-arginine administration, eight animals were sacrificed at 6 h and 9 h after LPS in group C and group LPS. The lungs were immediately removed for determination of surfactant-protein (SP-A) mRNA expression and broncho-alveolar lavage fluid (BALF). The total phospholipid (TPL) and total protein (TP) concentrations in the BALF were measured. Results SP-A mRNA in the lung tissue and TPL concentration in BALF were significantly decreased while TP concentration in BALF was significantly increased in group LPS, as compared with control groups( P < 0.01 ). L-arginine given at 3 h after LPS administration significantly attenuated the LPS-induced changes while L-arginine given at 6 h after LPS did not. Conclusion L-arginine can protect the lungs from LPS-induced injury by up-regulating PS-expression. Key words: Arginine; Endotoxemia; Respiratory distress syndrome, adult; Pulmonary surfactantassociated proteins
Key concepts: Lipopolysaccharide, Arginine, Pulmonary surfactant, Lung, Phospholipid, Respiratory distress, Medicine, Endocrinology