Intratracheal Atomization of Lipopolysaccharides Induced Lung Inflammatory Injury in Rats Model
LI Wei1,2,3, SHENG Yun-hua3, HANG Ai3, WANG Yu3, JIANG Zhu-hui3, ZHANG Su-hui3, TANG Li-ming3*
1. Fudan University, Shanghai 200120, China; 2. China state institute of pharmaceutical industry, Shanghai 200040, China; 3. Shanghai institute for food and drug control, Shanghai 201203, China
Abstract��OBJECTIVE To establish dose-related lung inflammatory injury in rats model with intratracheal atomization of lipopolysaccharide (lipopolysaccharides, LPS). METHODS Four groups of 4 rats were subjected to solvent or a single dose of LPS by intratracheal route using a IA-1B-2 inches-microsprayer. The male rats received 200 ��L solvent (control), LPS solutions (15, 5, 0.5 mg��kg-1). All rats were sacrificed 24 h after dose administration, biochemical analysis and cell counts on bronchoalveolar lavage fluid (BALF) were performed on each rat. Lung, trachea and kidney were examined histologically. Serum chemistry profiles of creatinine, ALB, Na, K, Cl- were detected. RESULTS Cell counts in BALF showed LPS groups had different degrees of inflammatory reaction. The alkaline phosphatase and total protein concentration were higher in LPS high dose group compared with other groups. In addition, the concentration of TNF-�� increased consistently with LPS dose and has statistical significance compared with the control group. Histopathology findings demonstrated that LPS produced an accumulation of foamy macrophages in the lungs and high degree of inflammation. CONCLUSION The results recommends intratracheally atomizing doses of LPS in rats model produced ranks of lung inflammatory injury.
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2017, Vol. 52 
